Polymorphic variants at NDUFC2, encoding a mitochondrial complex I subunit, associate with cardiac hypertrophy in human hypertension
Background A dysfunction of NADH dehydrogenase, the mitochondrial Complex I (CI), associated with the development of left ventricular hypertrophy (LVH) in previous experimental studies. A deficiency of Ndufc2 (subunit of CI) impairs CI activity causing severe mitochondrial dysfunction. The T allele...
Uloženo v:
| Vydáno v: | Molecular medicine (Cambridge, Mass.) Ročník 29; číslo 1; s. 107 - 13 |
|---|---|
| Hlavní autoři: | , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
London
BioMed Central
09.08.2023
Springer Nature B.V BMC |
| Témata: | |
| ISSN: | 1528-3658, 1076-1551, 1528-3658 |
| On-line přístup: | Získat plný text |
| Tagy: |
Přidat tag
Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!
|
| Abstract | Background
A dysfunction of NADH dehydrogenase, the mitochondrial Complex I (CI), associated with the development of left ventricular hypertrophy (LVH) in previous experimental studies. A deficiency of Ndufc2 (subunit of CI) impairs CI activity causing severe mitochondrial dysfunction. The T allele at
NDUFC2
/rs11237379 variant associates with reduced gene expression and impaired mitochondrial function. The present study tested the association of both
NDUFC2
/rs11237379 and NDUFC2/rs641836 variants with LVH in hypertensive patients. In vitro studies explored the impact of reduced Ndufc2 expression in isolated cardiomyocytes.
Methods
Two-hundred-forty-six subjects (147 male, 59.7%), with a mean age of 59 ± 15 years, were included for the genetic association analysis.
Ndufc2
silencing was performed in both H9c2 and rat primary cardiomyocytes to explore the hypertrophy development and the underlying signaling pathway.
Results
The TT genotype at
NDUFC2/
rs11237379 associated with significantly reduced gene expression. Multivariate analysis revealed that patients carrying this genotype showed significant differences for septal thickness (p = 0.07), posterior wall thickness (p = 0.008), RWT (p = 0.021), LV mass/BSA (p = 0.03), compared to subjects carrying either CC or CT genotypes. Patients carrying the A allele at
NDUFC2/
rs641836 showed significant differences for septal thickness (p = 0.017), posterior wall thickness (p = 0.011), LV mass (p = 0.003), LV mass/BSA (p = 0.002) and LV mass/height
2.7
(p = 0.010) after adjustment for covariates.
In-vitro
, the Ndufc2 deficiency-dependent mitochondrial dysfunction caused cardiomyocyte hypertrophy, pointing to SIRT3-AMPK-AKT-MnSOD as a major underlying signaling pathway.
Conclusions
We demonstrated for the first time a significant association of
NDUFC2
variants with LVH in human hypertension and highlight a key role of Ndufc2 deficiency-dependent CI mitochondrial dysfunction on increased susceptibility to cardiac hypertrophy development. |
|---|---|
| AbstractList | A dysfunction of NADH dehydrogenase, the mitochondrial Complex I (CI), associated with the development of left ventricular hypertrophy (LVH) in previous experimental studies. A deficiency of Ndufc2 (subunit of CI) impairs CI activity causing severe mitochondrial dysfunction. The T allele at NDUFC2/rs11237379 variant associates with reduced gene expression and impaired mitochondrial function. The present study tested the association of both NDUFC2/rs11237379 and NDUFC2/rs641836 variants with LVH in hypertensive patients. In vitro studies explored the impact of reduced Ndufc2 expression in isolated cardiomyocytes.
Two-hundred-forty-six subjects (147 male, 59.7%), with a mean age of 59 ± 15 years, were included for the genetic association analysis. Ndufc2 silencing was performed in both H9c2 and rat primary cardiomyocytes to explore the hypertrophy development and the underlying signaling pathway.
The TT genotype at NDUFC2/rs11237379 associated with significantly reduced gene expression. Multivariate analysis revealed that patients carrying this genotype showed significant differences for septal thickness (p = 0.07), posterior wall thickness (p = 0.008), RWT (p = 0.021), LV mass/BSA (p = 0.03), compared to subjects carrying either CC or CT genotypes. Patients carrying the A allele at NDUFC2/rs641836 showed significant differences for septal thickness (p = 0.017), posterior wall thickness (p = 0.011), LV mass (p = 0.003), LV mass/BSA (p = 0.002) and LV mass/height
(p = 0.010) after adjustment for covariates. In-vitro, the Ndufc2 deficiency-dependent mitochondrial dysfunction caused cardiomyocyte hypertrophy, pointing to SIRT3-AMPK-AKT-MnSOD as a major underlying signaling pathway.
We demonstrated for the first time a significant association of NDUFC2 variants with LVH in human hypertension and highlight a key role of Ndufc2 deficiency-dependent CI mitochondrial dysfunction on increased susceptibility to cardiac hypertrophy development. Abstract Background A dysfunction of NADH dehydrogenase, the mitochondrial Complex I (CI), associated with the development of left ventricular hypertrophy (LVH) in previous experimental studies. A deficiency of Ndufc2 (subunit of CI) impairs CI activity causing severe mitochondrial dysfunction. The T allele at NDUFC2/rs11237379 variant associates with reduced gene expression and impaired mitochondrial function. The present study tested the association of both NDUFC2/rs11237379 and NDUFC2/rs641836 variants with LVH in hypertensive patients. In vitro studies explored the impact of reduced Ndufc2 expression in isolated cardiomyocytes. Methods Two-hundred-forty-six subjects (147 male, 59.7%), with a mean age of 59 ± 15 years, were included for the genetic association analysis. Ndufc2 silencing was performed in both H9c2 and rat primary cardiomyocytes to explore the hypertrophy development and the underlying signaling pathway. Results The TT genotype at NDUFC2/rs11237379 associated with significantly reduced gene expression. Multivariate analysis revealed that patients carrying this genotype showed significant differences for septal thickness (p = 0.07), posterior wall thickness (p = 0.008), RWT (p = 0.021), LV mass/BSA (p = 0.03), compared to subjects carrying either CC or CT genotypes. Patients carrying the A allele at NDUFC2/rs641836 showed significant differences for septal thickness (p = 0.017), posterior wall thickness (p = 0.011), LV mass (p = 0.003), LV mass/BSA (p = 0.002) and LV mass/height2.7(p = 0.010) after adjustment for covariates. In-vitro, the Ndufc2 deficiency-dependent mitochondrial dysfunction caused cardiomyocyte hypertrophy, pointing to SIRT3-AMPK-AKT-MnSOD as a major underlying signaling pathway. Conclusions We demonstrated for the first time a significant association of NDUFC2 variants with LVH in human hypertension and highlight a key role of Ndufc2 deficiency-dependent CI mitochondrial dysfunction on increased susceptibility to cardiac hypertrophy development. A dysfunction of NADH dehydrogenase, the mitochondrial Complex I (CI), associated with the development of left ventricular hypertrophy (LVH) in previous experimental studies. A deficiency of Ndufc2 (subunit of CI) impairs CI activity causing severe mitochondrial dysfunction. The T allele at NDUFC2/rs11237379 variant associates with reduced gene expression and impaired mitochondrial function. The present study tested the association of both NDUFC2/rs11237379 and NDUFC2/rs641836 variants with LVH in hypertensive patients. In vitro studies explored the impact of reduced Ndufc2 expression in isolated cardiomyocytes.BACKGROUNDA dysfunction of NADH dehydrogenase, the mitochondrial Complex I (CI), associated with the development of left ventricular hypertrophy (LVH) in previous experimental studies. A deficiency of Ndufc2 (subunit of CI) impairs CI activity causing severe mitochondrial dysfunction. The T allele at NDUFC2/rs11237379 variant associates with reduced gene expression and impaired mitochondrial function. The present study tested the association of both NDUFC2/rs11237379 and NDUFC2/rs641836 variants with LVH in hypertensive patients. In vitro studies explored the impact of reduced Ndufc2 expression in isolated cardiomyocytes.Two-hundred-forty-six subjects (147 male, 59.7%), with a mean age of 59 ± 15 years, were included for the genetic association analysis. Ndufc2 silencing was performed in both H9c2 and rat primary cardiomyocytes to explore the hypertrophy development and the underlying signaling pathway.METHODSTwo-hundred-forty-six subjects (147 male, 59.7%), with a mean age of 59 ± 15 years, were included for the genetic association analysis. Ndufc2 silencing was performed in both H9c2 and rat primary cardiomyocytes to explore the hypertrophy development and the underlying signaling pathway.The TT genotype at NDUFC2/rs11237379 associated with significantly reduced gene expression. Multivariate analysis revealed that patients carrying this genotype showed significant differences for septal thickness (p = 0.07), posterior wall thickness (p = 0.008), RWT (p = 0.021), LV mass/BSA (p = 0.03), compared to subjects carrying either CC or CT genotypes. Patients carrying the A allele at NDUFC2/rs641836 showed significant differences for septal thickness (p = 0.017), posterior wall thickness (p = 0.011), LV mass (p = 0.003), LV mass/BSA (p = 0.002) and LV mass/height2.7(p = 0.010) after adjustment for covariates. In-vitro, the Ndufc2 deficiency-dependent mitochondrial dysfunction caused cardiomyocyte hypertrophy, pointing to SIRT3-AMPK-AKT-MnSOD as a major underlying signaling pathway.RESULTSThe TT genotype at NDUFC2/rs11237379 associated with significantly reduced gene expression. Multivariate analysis revealed that patients carrying this genotype showed significant differences for septal thickness (p = 0.07), posterior wall thickness (p = 0.008), RWT (p = 0.021), LV mass/BSA (p = 0.03), compared to subjects carrying either CC or CT genotypes. Patients carrying the A allele at NDUFC2/rs641836 showed significant differences for septal thickness (p = 0.017), posterior wall thickness (p = 0.011), LV mass (p = 0.003), LV mass/BSA (p = 0.002) and LV mass/height2.7(p = 0.010) after adjustment for covariates. In-vitro, the Ndufc2 deficiency-dependent mitochondrial dysfunction caused cardiomyocyte hypertrophy, pointing to SIRT3-AMPK-AKT-MnSOD as a major underlying signaling pathway.We demonstrated for the first time a significant association of NDUFC2 variants with LVH in human hypertension and highlight a key role of Ndufc2 deficiency-dependent CI mitochondrial dysfunction on increased susceptibility to cardiac hypertrophy development.CONCLUSIONSWe demonstrated for the first time a significant association of NDUFC2 variants with LVH in human hypertension and highlight a key role of Ndufc2 deficiency-dependent CI mitochondrial dysfunction on increased susceptibility to cardiac hypertrophy development. BackgroundA dysfunction of NADH dehydrogenase, the mitochondrial Complex I (CI), associated with the development of left ventricular hypertrophy (LVH) in previous experimental studies. A deficiency of Ndufc2 (subunit of CI) impairs CI activity causing severe mitochondrial dysfunction. The T allele at NDUFC2/rs11237379 variant associates with reduced gene expression and impaired mitochondrial function. The present study tested the association of both NDUFC2/rs11237379 and NDUFC2/rs641836 variants with LVH in hypertensive patients. In vitro studies explored the impact of reduced Ndufc2 expression in isolated cardiomyocytes.MethodsTwo-hundred-forty-six subjects (147 male, 59.7%), with a mean age of 59 ± 15 years, were included for the genetic association analysis. Ndufc2 silencing was performed in both H9c2 and rat primary cardiomyocytes to explore the hypertrophy development and the underlying signaling pathway.ResultsThe TT genotype at NDUFC2/rs11237379 associated with significantly reduced gene expression. Multivariate analysis revealed that patients carrying this genotype showed significant differences for septal thickness (p = 0.07), posterior wall thickness (p = 0.008), RWT (p = 0.021), LV mass/BSA (p = 0.03), compared to subjects carrying either CC or CT genotypes. Patients carrying the A allele at NDUFC2/rs641836 showed significant differences for septal thickness (p = 0.017), posterior wall thickness (p = 0.011), LV mass (p = 0.003), LV mass/BSA (p = 0.002) and LV mass/height2.7(p = 0.010) after adjustment for covariates. In-vitro, the Ndufc2 deficiency-dependent mitochondrial dysfunction caused cardiomyocyte hypertrophy, pointing to SIRT3-AMPK-AKT-MnSOD as a major underlying signaling pathway.ConclusionsWe demonstrated for the first time a significant association of NDUFC2 variants with LVH in human hypertension and highlight a key role of Ndufc2 deficiency-dependent CI mitochondrial dysfunction on increased susceptibility to cardiac hypertrophy development. Background A dysfunction of NADH dehydrogenase, the mitochondrial Complex I (CI), associated with the development of left ventricular hypertrophy (LVH) in previous experimental studies. A deficiency of Ndufc2 (subunit of CI) impairs CI activity causing severe mitochondrial dysfunction. The T allele at NDUFC2 /rs11237379 variant associates with reduced gene expression and impaired mitochondrial function. The present study tested the association of both NDUFC2 /rs11237379 and NDUFC2/rs641836 variants with LVH in hypertensive patients. In vitro studies explored the impact of reduced Ndufc2 expression in isolated cardiomyocytes. Methods Two-hundred-forty-six subjects (147 male, 59.7%), with a mean age of 59 ± 15 years, were included for the genetic association analysis. Ndufc2 silencing was performed in both H9c2 and rat primary cardiomyocytes to explore the hypertrophy development and the underlying signaling pathway. Results The TT genotype at NDUFC2/ rs11237379 associated with significantly reduced gene expression. Multivariate analysis revealed that patients carrying this genotype showed significant differences for septal thickness (p = 0.07), posterior wall thickness (p = 0.008), RWT (p = 0.021), LV mass/BSA (p = 0.03), compared to subjects carrying either CC or CT genotypes. Patients carrying the A allele at NDUFC2/ rs641836 showed significant differences for septal thickness (p = 0.017), posterior wall thickness (p = 0.011), LV mass (p = 0.003), LV mass/BSA (p = 0.002) and LV mass/height 2.7 (p = 0.010) after adjustment for covariates. In-vitro , the Ndufc2 deficiency-dependent mitochondrial dysfunction caused cardiomyocyte hypertrophy, pointing to SIRT3-AMPK-AKT-MnSOD as a major underlying signaling pathway. Conclusions We demonstrated for the first time a significant association of NDUFC2 variants with LVH in human hypertension and highlight a key role of Ndufc2 deficiency-dependent CI mitochondrial dysfunction on increased susceptibility to cardiac hypertrophy development. |
| ArticleNumber | 107 |
| Author | Marchitti, Simona Bianchi, Franca Stanzione, Rosita Cotugno, Maria Forte, Maurizio Frati, Giacomo Rubattu, Speranza Scioli, Mariarosaria Barbato, Emanuele Palmerio, Silvia Gallo, Giovanna Sciarretta, Sebastiano Tocci, Giuliano Volpe, Massimo |
| Author_xml | – sequence: 1 givenname: Giovanna surname: Gallo fullname: Gallo, Giovanna organization: Department of Clinical and Molecular Medicine, School of Medicine and Psychology, Sapienza University – sequence: 2 givenname: Maurizio surname: Forte fullname: Forte, Maurizio organization: IRCCS Neuromed – sequence: 3 givenname: Maria surname: Cotugno fullname: Cotugno, Maria organization: IRCCS Neuromed – sequence: 4 givenname: Simona surname: Marchitti fullname: Marchitti, Simona organization: IRCCS Neuromed – sequence: 5 givenname: Rosita surname: Stanzione fullname: Stanzione, Rosita organization: IRCCS Neuromed – sequence: 6 givenname: Giuliano surname: Tocci fullname: Tocci, Giuliano organization: Department of Clinical and Molecular Medicine, School of Medicine and Psychology, Sapienza University – sequence: 7 givenname: Franca surname: Bianchi fullname: Bianchi, Franca organization: IRCCS Neuromed – sequence: 8 givenname: Silvia surname: Palmerio fullname: Palmerio, Silvia organization: Department of Medicine, University of Verona School of Medicine, Verona University Hospital Trust – sequence: 9 givenname: Mariarosaria surname: Scioli fullname: Scioli, Mariarosaria organization: IRCCS Neuromed – sequence: 10 givenname: Giacomo surname: Frati fullname: Frati, Giacomo organization: IRCCS Neuromed, Department of Medical-Surgical Sciences and Biotechnologies, Sapienza University of Rome – sequence: 11 givenname: Sebastiano surname: Sciarretta fullname: Sciarretta, Sebastiano organization: IRCCS Neuromed, Department of Medical-Surgical Sciences and Biotechnologies, Sapienza University of Rome – sequence: 12 givenname: Emanuele surname: Barbato fullname: Barbato, Emanuele organization: Department of Clinical and Molecular Medicine, School of Medicine and Psychology, Sapienza University – sequence: 13 givenname: Massimo surname: Volpe fullname: Volpe, Massimo organization: Department of Clinical and Molecular Medicine, School of Medicine and Psychology, Sapienza University, IRCCS S. Raffaele – sequence: 14 givenname: Speranza orcidid: 0000-0001-5921-7368 surname: Rubattu fullname: Rubattu, Speranza email: speranzadonatella.rubattu@uniroma1.it organization: Department of Clinical and Molecular Medicine, School of Medicine and Psychology, Sapienza University, IRCCS Neuromed |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/37558995$$D View this record in MEDLINE/PubMed |
| BookMark | eNp9kk1vFCEcxiemxr7oF_BgSLx46CjMAMOcTLNa3aRRD_ZMGF522MzACEzdvfvBZbtbbXvoCfjze548gee0OHLe6aJ4jeB7hBj9EBGEFSxhVZcQNhCVm2fFCSIVK2tK2NG9_XFxGuM604hg8qI4rhtCWNuSk-LPDz9sRx-m3kpwI4IVLkUgEvj26fpyUZ0D7aRX1q2AAKNNXvbeqUwNQPpxGvQGLEGcu9nZdA5EjF5akTT4bVMPpAjKCgn67aRDCn7qt8A60M-jcIehdtF697J4bsQQ9avDelZcX37-ufhaXn3_slxcXJWS4iqVRncdNcpojGrUaYYwaw1VRDWGmSofaGeMlhR1uEGSwg4JhGglmEIGS0Tqs2K591VerPkU7CjClnth-e3AhxUXIVk5aN5SRFrW1VC2BhvDBBW0U0QQRVupW529Pu69prkbtZLapSCGB6YPb5zt-crfcAQxggzR7PDu4BD8r1nHxEcbpR4G4bSfI68YZgxjQnbB3z5C134OLr_VjmpZAyHDmXpzP9K_LHe_nQG2B2TwMQZtuLRJpPwDOaEdcjS-KxbfF4vnYvHbYvFNllaPpHfuT4rqvShm2K10-B_7CdVfXMDj5A |
| CitedBy_id | crossref_primary_10_3390_ijms25126661 crossref_primary_10_3390_biomedicines11123109 crossref_primary_10_1007_s11010_024_05074_1 crossref_primary_10_1016_j_bbadis_2024_167249 crossref_primary_10_3390_ijms25052667 |
| Cites_doi | 10.1371/journal.pone.0094157 10.1016/j.echo.2014.10.003 10.1155/2021/5545261 10.3390/cells8101149 10.1161/01.CIR.102.4.470 10.1080/15548627.2019.1687215 10.1161/JAHA.115.002701 10.1161/01.RES.84.6.722 10.1021/pr801059u 10.1038/s12276-019-0355-7 10.3389/fcvm.2022.921244 10.1161/CIRCRESAHA.118.312498 10.1016/j.carpath.2013.11.002 10.1093/hmg/ddx333 10.1074/jbc.M109.077271 10.1080/15548627.2022.2115675 10.1161/01.HYP.0000118584.33350.7d 10.1007/s11897-012-0109-5 10.1016/j.ijcard.2019.02.027 10.1016/j.yjmcc.2012.09.002 10.1093/eurheartj/ehy339 10.1093/gbe/evu208 10.1093/cvr/cvq250 10.1038/s41569-018-0007-y |
| ContentType | Journal Article |
| Copyright | The Author(s) 2023 2023. The Feinstein Institute for Medical Research. 2023. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. The Feinstein Institute for Medical Research 2023 |
| Copyright_xml | – notice: The Author(s) 2023 – notice: 2023. The Feinstein Institute for Medical Research. – notice: 2023. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. – notice: The Feinstein Institute for Medical Research 2023 |
| DBID | C6C AAYXX CITATION CGR CUY CVF ECM EIF NPM 3V. 7X7 7XB 8FI 8FJ 8FK ABUWG AFKRA AZQEC BENPR CCPQU DWQXO FYUFA GHDGH K9. M0S PHGZM PHGZT PIMPY PJZUB PKEHL PPXIY PQEST PQQKQ PQUKI 7X8 5PM DOA |
| DOI | 10.1186/s10020-023-00701-x |
| DatabaseName | Springer Nature OA Free Journals CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed ProQuest Central (Corporate) Health & Medical Collection ProQuest Central (purchase pre-March 2016) ProQuest Hospital Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) ProQuest Central (Alumni) ProQuest Central UK/Ireland ProQuest Central Essentials ProQuest Central ProQuest One ProQuest Central Korea Proquest Health Research Premium Collection Health Research Premium Collection (Alumni) ProQuest Health & Medical Complete (Alumni) ProQuest Health & Medical Collection ProQuest Central Premium ProQuest One Academic (New) Publicly Available Content Database ProQuest Health & Medical Research Collection ProQuest One Academic Middle East (New) ProQuest One Health & Nursing ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Academic (retired) ProQuest One Academic UKI Edition MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Publicly Available Content Database ProQuest One Academic Middle East (New) ProQuest Central Essentials ProQuest One Academic Eastern Edition ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) ProQuest One Community College ProQuest Hospital Collection Health Research Premium Collection (Alumni) ProQuest One Health & Nursing ProQuest Hospital Collection (Alumni) ProQuest Central ProQuest Health & Medical Complete ProQuest Health & Medical Research Collection Health Research Premium Collection ProQuest One Academic UKI Edition Health and Medicine Complete (Alumni Edition) ProQuest Central Korea ProQuest Central (New) ProQuest One Academic ProQuest One Academic (New) ProQuest Central (Alumni) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE MEDLINE - Academic Publicly Available Content Database |
| Database_xml | – sequence: 1 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 3 dbid: PIMPY name: ProQuest Publicly Available Content Database url: http://search.proquest.com/publiccontent sourceTypes: Aggregation Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Biology |
| EISSN | 1528-3658 |
| EndPage | 13 |
| ExternalDocumentID | oai_doaj_org_article_961598b30c9f4ff8a6a6bd5a5d69ce9e PMC10410816 37558995 10_1186_s10020_023_00701_x |
| Genre | Journal Article |
| GeographicLocations | United States--US Italy |
| GeographicLocations_xml | – name: United States--US – name: Italy |
| GroupedDBID | --- -ET 0R~ 123 29M 2WC 36B 5RE 5VS 7X7 8FI 8FJ AAFWJ AAJSJ AASML ABUWG ACGFO ACMJI ADBBV ADUKV AEGXH AENEX AFKRA AFPKN AIAGR ALMA_UNASSIGNED_HOLDINGS AMKLP AMTXH AOIJS BAPOH BAWUL BCNDV BENPR BFQNJ BMC C6C CCPQU CS3 DIK DU5 E3Z EBD EBLON EBS EMB EMOBN F5P FYUFA GROUPED_DOAJ GX1 HH5 HMCUK HYE IAO IH2 IHR ISR ITC KQ8 LGEZI LOTEE NADUK NXXTH OK1 OVT P2P PHGZM PHGZT PIMPY PUEGO RBZ RNS ROL RPM RSV SDH SJN SOJ SV3 TR2 UKHRP WOQ AAYXX AFFHD CITATION ALIPV CGR CUY CVF ECM EIF NPM 3V. 7XB 8FK AZQEC DWQXO K9. PJZUB PKEHL PPXIY PQEST PQQKQ PQUKI 7X8 5PM |
| ID | FETCH-LOGICAL-c642t-febb6fdfe4131be81489f6d5d7f8f24896bffec61b471c60b1a1162a8d1f4c153 |
| IEDL.DBID | DOA |
| ISICitedReferencesCount | 6 |
| ISICitedReferencesURI | http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=001044368900001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| ISSN | 1528-3658 1076-1551 |
| IngestDate | Fri Oct 03 12:38:17 EDT 2025 Tue Nov 04 02:06:13 EST 2025 Sun Nov 09 10:27:44 EST 2025 Sun Oct 19 01:27:31 EDT 2025 Thu Apr 03 07:01:22 EDT 2025 Tue Nov 18 21:23:56 EST 2025 Sat Nov 29 02:40:47 EST 2025 Sat Sep 06 07:22:12 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 1 |
| Keywords | Hypertension Cardiac hypertrophy Mitochondrial complex I Mitochondrial dysfunction SIRT3 NDUFC2 |
| Language | English |
| License | 2023. The Feinstein Institute for Medical Research. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c642t-febb6fdfe4131be81489f6d5d7f8f24896bffec61b471c60b1a1162a8d1f4c153 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
| ORCID | 0000-0001-5921-7368 |
| OpenAccessLink | https://doaj.org/article/961598b30c9f4ff8a6a6bd5a5d69ce9e |
| PMID | 37558995 |
| PQID | 2849870084 |
| PQPubID | 5066171 |
| PageCount | 13 |
| ParticipantIDs | doaj_primary_oai_doaj_org_article_961598b30c9f4ff8a6a6bd5a5d69ce9e pubmedcentral_primary_oai_pubmedcentral_nih_gov_10410816 proquest_miscellaneous_2848844555 proquest_journals_2849870084 pubmed_primary_37558995 crossref_citationtrail_10_1186_s10020_023_00701_x crossref_primary_10_1186_s10020_023_00701_x springer_journals_10_1186_s10020_023_00701_x |
| PublicationCentury | 2000 |
| PublicationDate | 2023-08-09 |
| PublicationDateYYYYMMDD | 2023-08-09 |
| PublicationDate_xml | – month: 08 year: 2023 text: 2023-08-09 day: 09 |
| PublicationDecade | 2020 |
| PublicationPlace | London |
| PublicationPlace_xml | – name: London – name: England – name: New York |
| PublicationTitle | Molecular medicine (Cambridge, Mass.) |
| PublicationTitleAbbrev | Mol Med |
| PublicationTitleAlternate | Mol Med |
| PublicationYear | 2023 |
| Publisher | BioMed Central Springer Nature B.V BMC |
| Publisher_xml | – name: BioMed Central – name: Springer Nature B.V – name: BMC |
| References | MG Rosca (701_CR19) 2013; 55 F Kuwahara (701_CR8) 2004; 43 W Zhang (701_CR25) 1999; 84 BH Lorell (701_CR10) 2000; 102 G Gallo (701_CR5) 2022; 9 VB Pillai (701_CR16) 2010; 285 JN Peoples (701_CR14) 2019; 51 M Gershoni (701_CR6) 2014; 6 C Meng (701_CR11) 2009; 8 B Williams (701_CR24) 2018; 39 S Raffa (701_CR18) 2019; 286 701_CR20 VB Pillai (701_CR15) 2010; 88 NR Sundaresan (701_CR21) 2009; 119 R Zou (701_CR26) 2021; 2021 701_CR4 701_CR1 AE Kane (701_CR7) 2018; 123 RM Lang (701_CR9) 2015; 28 L van Heerebeek (701_CR23) 2012; 9 S Raffa (701_CR17) 2017; 26 M Nakamura (701_CR12) 2018; 15 M Forte (701_CR2) 2019; 97 M Forte (701_CR3) 2020; 16 701_CR13 Y Tang (701_CR22) 2014; 23 |
| References_xml | – ident: 701_CR1 doi: 10.1371/journal.pone.0094157 – volume: 119 start-page: 2758 year: 2009 ident: 701_CR21 publication-title: J Clin Invest – volume: 28 start-page: 1 year: 2015 ident: 701_CR9 publication-title: J Am Soc Echocardiogr doi: 10.1016/j.echo.2014.10.003 – volume: 2021 start-page: 5545261 year: 2021 ident: 701_CR26 publication-title: Oxid Med Cell Longev doi: 10.1155/2021/5545261 – ident: 701_CR13 doi: 10.3390/cells8101149 – volume: 102 start-page: 470 year: 2000 ident: 701_CR10 publication-title: Circulation doi: 10.1161/01.CIR.102.4.470 – volume: 16 start-page: 1468 year: 2020 ident: 701_CR3 publication-title: Autophagy doi: 10.1080/15548627.2019.1687215 – ident: 701_CR20 doi: 10.1161/JAHA.115.002701 – volume: 84 start-page: 722 year: 1999 ident: 701_CR25 publication-title: Circ Res doi: 10.1161/01.RES.84.6.722 – volume: 8 start-page: 2463 year: 2009 ident: 701_CR11 publication-title: J Proteome Res doi: 10.1021/pr801059u – volume: 51 start-page: 1 year: 2019 ident: 701_CR14 publication-title: Exp Mol Med doi: 10.1038/s12276-019-0355-7 – volume: 9 start-page: 921244 year: 2022 ident: 701_CR5 publication-title: Front Cardiovasc Med doi: 10.3389/fcvm.2022.921244 – volume: 123 start-page: 868 year: 2018 ident: 701_CR7 publication-title: Circ Res doi: 10.1161/CIRCRESAHA.118.312498 – volume: 23 start-page: 101 year: 2014 ident: 701_CR22 publication-title: Cardiovasc Pathol doi: 10.1016/j.carpath.2013.11.002 – volume: 26 start-page: 4541 year: 2017 ident: 701_CR17 publication-title: Hum Mol Genet doi: 10.1093/hmg/ddx333 – volume: 97 start-page: 579 year: 2019 ident: 701_CR2 publication-title: J Mol Med (Berl) – volume: 285 start-page: 3133 year: 2010 ident: 701_CR16 publication-title: J Biol Chem doi: 10.1074/jbc.M109.077271 – ident: 701_CR4 doi: 10.1080/15548627.2022.2115675 – volume: 43 start-page: 739 year: 2004 ident: 701_CR8 publication-title: Hypertension doi: 10.1161/01.HYP.0000118584.33350.7d – volume: 9 start-page: 293 year: 2012 ident: 701_CR23 publication-title: Curr Heart Fail Rep doi: 10.1007/s11897-012-0109-5 – volume: 286 start-page: 127 year: 2019 ident: 701_CR18 publication-title: Int J Cardiol doi: 10.1016/j.ijcard.2019.02.027 – volume: 55 start-page: 31 year: 2013 ident: 701_CR19 publication-title: J Mol Cell Cardiol doi: 10.1016/j.yjmcc.2012.09.002 – volume: 39 start-page: 3021 year: 2018 ident: 701_CR24 publication-title: Eur Heart J doi: 10.1093/eurheartj/ehy339 – volume: 6 start-page: 2665 year: 2014 ident: 701_CR6 publication-title: Genome Biol Evol doi: 10.1093/gbe/evu208 – volume: 88 start-page: 250 year: 2010 ident: 701_CR15 publication-title: Cardiovasc Res doi: 10.1093/cvr/cvq250 – volume: 15 start-page: 387 year: 2018 ident: 701_CR12 publication-title: Nat Rev Cardiol doi: 10.1038/s41569-018-0007-y |
| SSID | ssj0021545 |
| Score | 2.431838 |
| Snippet | Background
A dysfunction of NADH dehydrogenase, the mitochondrial Complex I (CI), associated with the development of left ventricular hypertrophy (LVH) in... A dysfunction of NADH dehydrogenase, the mitochondrial Complex I (CI), associated with the development of left ventricular hypertrophy (LVH) in previous... BackgroundA dysfunction of NADH dehydrogenase, the mitochondrial Complex I (CI), associated with the development of left ventricular hypertrophy (LVH) in... Abstract Background A dysfunction of NADH dehydrogenase, the mitochondrial Complex I (CI), associated with the development of left ventricular hypertrophy... |
| SourceID | doaj pubmedcentral proquest pubmed crossref springer |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 107 |
| SubjectTerms | Adult Aged Animals Biomedical and Life Sciences Biomedicine Cardiac hypertrophy Cardiology Cardiomegaly - genetics Cardiomyocytes Cardiovascular disease Diuretics Electron Transport Complex I - genetics Genotype Heart Humans Hypertension Hypertension - complications Hypertension - genetics Hypertrophy, Left Ventricular - complications Hypertrophy, Left Ventricular - genetics Male Middle Aged Mitochondrial complex I Mitochondrial dysfunction Molecular Medicine NDUFC2 Oxidative stress Rats Research Article Signal Transduction SIRT3 Stroke |
| SummonAdditionalLinks | – databaseName: Health & Medical Collection dbid: 7X7 link: http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1Lb9QwELaggMSFdyFQkJG4sRFJGj9yQlBYwWXVA5X2Zjl-0JXapGSz1fbOD2fGcXa1PHrhmNiRnMw3j8-ezBDyxnrBtBM5aJqr07IwItXC6dRluuKSVd5KE5pNiNlMzufVcdxwW8a0ytEmBkNtW4N75O_AjAI9xvLv7y9-pNg1Ck9XYwuNm-QWts1GnIv5lnBheDDkHPIUQ4PxpxnJ8dc5JE7gsVKseJOn6x3HFOr3_y3o_DN38rcD1OCXpvf_940ekHsxIqUfBgg9JDdc84jcGXpUXj0mP4_bs6vzFsSxMPQSmDUmzlDd09mnk-lRMaFYCRMdINX0HMwDmNPGIqppyFZ3a_qVLlf1CkzHhOoIBkdx_5eaAE9DT4EMd33XgsjpoqGhb2C8ifn1bfOEnEw_fzv6ksbWDakBQtOn3tU199Y78JF57SSQrspzy6zw0hdwwWtMV-F5Dc7R8KzOdZ7zQkub-9KAFd4ne03buGeEaogxSiaB9Je25IWVTtjMGOYzYT042YTko9yUiXXNsb3GmQr8RnI1yFqBrFWQtVon5O3mmYuhqse1sz8iHDYzsSJ3uNF231VUcFVBaFjJ-jAzlS-9l5prXlummeWVcZVLyMGIAhXNxFJtIZCQ15thUHA8tdGNa1dhjpRlyRhLyNMBe5uVHArGgDDDiNxB5c5Sd0eaxWkoIg40PMemKwmZjADeruvf3-L59a_xgtwtgk5hTs0B2eu7lXtJbpvLfrHsXgXt_AXdQ0OB priority: 102 providerName: ProQuest – databaseName: Springer LINK dbid: RSV link: http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Lb9QwELZQAYkLlHegICNxYyPFafw6QtsVXFYVUNSb5SddqU1QNlu19_5wxs4DLS1IcEzsSNb4m8cXj2cQeusCp9pzAprmTV6Vlueae537QksmqAxO2NRsgi8W4vhYHg6XwlZjtvt4JJksdVJrweJlt0h1wMfksUYNySFyvA3uTsSGDZ-_fJtoVgwKxusxN3634YJSpf6bwsvrWZK_HZUmDzR_8H9r30b3h4gTv-8h8hDd8vUjdLfvQXn5GF0dNqfA_0HcS4vPgTnHxBisO7zYP5rvlTMcK11GB4c1PgP1B3NZu4hanLLR_QX-hFdrswbTMMN62GyP4_9dbBP8LD4Bstt2bQNbipc1Tn0Bh5cxf76pn6Cj-cHXvY_50Joht0BYujx4Y1hwwYMPJMYLIFUyMEcdDyKU8MBMTEdhxIDzs6wwRBPCSi0cCZUFK_sUbdVN7Z8jrCGGqKgAUl-5ipVOeO4Ka2kouAvgRDNExt1SdqhbHttnnKrEXwRTvXQVSFcl6aqLDL2bvvnRV-346-wPEQTTzFhxO71o2u9qUGAlIfSTwuwWVoYqBKGZZsZRTR2T1kufoZ0RQmowAysFvl-CQSxElaE30zAocDyV0bVv1mmOEFVFKc3Qsx5x00p2OaVAiGFEbGBxY6mbI_XyJBUJB5pNYlOVDM1GSP5a159l8eLfpr9E98qE6phDs4O2unbtX6E79rxbrtrXSS9_At9HOD0 priority: 102 providerName: Springer Nature |
| Title | Polymorphic variants at NDUFC2, encoding a mitochondrial complex I subunit, associate with cardiac hypertrophy in human hypertension |
| URI | https://link.springer.com/article/10.1186/s10020-023-00701-x https://www.ncbi.nlm.nih.gov/pubmed/37558995 https://www.proquest.com/docview/2849870084 https://www.proquest.com/docview/2848844555 https://pubmed.ncbi.nlm.nih.gov/PMC10410816 https://doaj.org/article/961598b30c9f4ff8a6a6bd5a5d69ce9e |
| Volume | 29 |
| WOSCitedRecordID | wos001044368900001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| journalDatabaseRights | – providerCode: PRVADU databaseName: BioMed Central Open Access Free customDbUrl: eissn: 1528-3658 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0021545 issn: 1528-3658 databaseCode: RBZ dateStart: 20180101 isFulltext: true titleUrlDefault: https://www.biomedcentral.com/search/ providerName: BioMedCentral – providerCode: PRVAON databaseName: DOAJ Directory of Open Access Journals customDbUrl: eissn: 1528-3658 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0021545 issn: 1528-3658 databaseCode: DOA dateStart: 20000101 isFulltext: true titleUrlDefault: https://www.doaj.org/ providerName: Directory of Open Access Journals – providerCode: PRVPQU databaseName: Health & Medical Collection customDbUrl: eissn: 1528-3658 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0021545 issn: 1528-3658 databaseCode: 7X7 dateStart: 20110101 isFulltext: true titleUrlDefault: https://search.proquest.com/healthcomplete providerName: ProQuest – providerCode: PRVPQU databaseName: ProQuest Central customDbUrl: eissn: 1528-3658 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0021545 issn: 1528-3658 databaseCode: BENPR dateStart: 20110101 isFulltext: true titleUrlDefault: https://www.proquest.com/central providerName: ProQuest – providerCode: PRVPQU databaseName: ProQuest Publicly Available Content Database customDbUrl: eissn: 1528-3658 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0021545 issn: 1528-3658 databaseCode: PIMPY dateStart: 20110101 isFulltext: true titleUrlDefault: http://search.proquest.com/publiccontent providerName: ProQuest – providerCode: PRVAVX databaseName: Springer LINK customDbUrl: eissn: 1528-3658 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0021545 issn: 1528-3658 databaseCode: RSV dateStart: 19970101 isFulltext: true titleUrlDefault: https://link.springer.com/search?facet-content-type=%22Journal%22 providerName: Springer Nature |
| link | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Jj9MwFLZgAIkLYicwVEbiRiPiTLwdmWEq5kBVDQwqJ8urptKQoDYdlTs_nGcnKZT1wiWSY0ey3uLPX_z8HkLPXeBUe07A07zJq9LyXHOvc19oyQSVwQmbik3w6VTM53L2Q6mvGBPWpQfuBPdSAuRKYQ4KK0MVgtBMM-Oopo5J66WPq2_B5UCmeqoVNwbDFRnB4kW5SJMAn_KY34bkmx0YStn6f7fF_DVS8qfj0oRCk9voVr99xK-6ad9BV3x9F93oCkp-uYe-zpoLIPMgu4XFl0CDY5QL1i2evj6bHJVjHNNWRrTCGn8CX4a1r3bRBHEKLfcbfIJXa7MGPx9j3WvO4_izFttkSxafA3NdtssG9IMXNU5F_vqXMRi-qe-js8nx-6M3eV9nIbfAPto8eGNYcMEDoBHjBTAkGZijjgcRSmgwE2NLGDGAZJYVhmhCWKmFI6GysGQ-QHt1U_tHCGvYEFRUAEOvXMVKJzx3hbU0FNwFQMQMkUHsyvZJyGMtjAuVyIhgqlOVAlWppCq1ydCL7TefuxQcfx19GLW5HRnTZ6cXYFSqNyr1L6PK0P5gC6r36ZUCIJewuhWiytCzbTd4Yzxi0bVv1mmMEFVFKc3Qw850tjM54JQCu4UesWNUO1Pd7akX5ynjN3BmEiukZGg82N_3ef1ZFo__hyyeoJtlcpwYJrOP9trl2j9F1-1lu1gtR-gqn_P0FCN07fB4OjsdJVeE1uzk7ewjtE7fffgG0eA62w |
| linkProvider | Directory of Open Access Journals |
| linkToHtml | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V1Lb9NAEF5VBQQX3o9AgUWCE7Hqdbzr9QEhaIkatUQ9tFJuZr0PGqm1S-KU5M7v4Tcys7YThUdvPXCMdyNtNt98M-OdnY-Q18YlXNmEgaXZPIgjnQQqsSqwoUqF5KkzUnuxiWQ4lKNRerhBfrZ3YbCssuVET9Sm1PiOfBtoFNJjbP_-_vxbgKpReLraSmjUsNi3i--Qsk3fDXbh_30TRf1PRzt7QaMqEGiItavA2TwXzjgL9M1yKyEfSJ0w3CROugg-iBwrKQTLgbe1CHOmGBORkoa5WDNUiQDKvwY8nmCyl4xWCR6GI3WNowgwFGkv6UiBV_UwUQMPGWCHHRbM1xyh1wv4W5D7Z63mbwe23g_27_xvO3iX3G4ibvqhNpF7ZMMW98mNWoNz8YD8OCxPF2clwG2s6YUCeyyqKVUVHe4e93eiLsVOn-jgqaJnQH_gLgqDVkt9Nb6d0wGdzvIZUGOXqgbsluL7baq9-Wl6Asn-pJqUAGk6LqjXRWwe4v2BsnhIjq9kCx6RzaIs7BNCFcRQMZc278UmFpGRNjGh1tyFiXEQRHQIa3GS6aZvO8qHnGY-f5Miq7GVAbYyj61s3iFvl985r7uWXDr7I8JvORM7jvsH5eRr1hBYlkLom8q8F-rUxc5JJZTIDVfciFTb1HbIVou6rKHBabaCXIe8Wg4DgeGplCpsOfNzpIxjznmHPK6xvlxJL-FcpimMyDUrWFvq-kgxPvFN0lkYMxSV6ZBuazCrdf17L55e_jNekpt7R58PsoPBcP8ZuRV5e8b6oS2yWU1m9jm5ri-q8XTywjMDJV-u2pB-AQbdong |
| linkToPdf | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V1Lj9MwELZWXUBceD8CCxgJTjTaOI0d-4AQbKmoFqoeWGk5ZR0_2Eq7SWnTpb3zq_h1jJ2kq_LY2x44NnYl1_2-b2bi8QxCL7RNqTQpAaaZPExilYYyNTI0kRSMU2E1V77ZRDoa8cNDMd5CP9u7MC6tstVEL9S6VO4d-S7IKITHrvz7rm3SIsb9wZvpt9B1kHInrW07jRoi-2b1HcK3-ethH_7rl3E8eP9570PYdBgIFfjdVWhNnjOrrQEpJ7nhEBsIyzTVqeU2hg8sd1kVjOSg4YpFOZGEsFhyTWyiiOsYAfK_DS55EnfQ9nj4afxlHe4556TOeGShc0zaKzucuYt7LmwDexm6ejskXG6YRd894G8u75-Zm78d33qrOLj5P-_nLXSj8cXx25o8t9GWKe6gq3V3ztVd9GNcnqxOSwDiROEzCUwtqjmWFR71DwZ7cRe7GqDO9GOJT0EYwZAU2vEZ-zx9s8RDPF_kCxDNLpYNDQx2b76x8sRU-Hg1NbNqVgLY8aTAvmNi89DdLCiLe-jgUrbgPuoUZWEeIizBu0ooN3kv0QmLNTepjpSiNkq1BfciQKTFTKaaiu6uschJ5iM7zrIaZxngLPM4y5YBerX-zrSuZ3Lh7HcOiuuZrha5f1DOvmaNtGUCnGLB816khE2s5ZJJlmsqqWZCGWECtNMiMGsEcp6dwy9Az9fDIG3uvEoWplz4OZwnCaU0QA9q3K9X0ksp5ULACN9gxMZSN0eKybEvn06ihLh2MwHqtuQ5X9e_9-LRxT_jGboG_Mk-Dkf7j9H12FPbJRbtoE41W5gn6Io6qybz2dNGJjA6umwm_QJtvKzH |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Polymorphic+variants+at+NDUFC2%2C+encoding+a+mitochondrial+complex+I+subunit%2C+associate+with+cardiac+hypertrophy+in+human+hypertension&rft.jtitle=Molecular+medicine+%28Cambridge%2C+Mass.%29&rft.au=Giovanna+Gallo&rft.au=Maurizio+Forte&rft.au=Maria+Cotugno&rft.au=Simona+Marchitti&rft.date=2023-08-09&rft.pub=BMC&rft.eissn=1528-3658&rft.volume=29&rft.issue=1&rft.spage=1&rft.epage=13&rft_id=info:doi/10.1186%2Fs10020-023-00701-x&rft.externalDBID=DOA&rft.externalDocID=oai_doaj_org_article_961598b30c9f4ff8a6a6bd5a5d69ce9e |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1528-3658&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1528-3658&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1528-3658&client=summon |