Extracellular Nicotinamide Phosphoribosyltransferase Is a Component of the Senescence-Associated Secretory Phenotype

Cellular senescence is a stress or damage response by which a cell adopts of state of essentially permanent proliferative arrest, coupled to the secretion of a number of biologically active molecules. This senescence-associated secretory phenotype (SASP) underlies many of the degenerative and regene...

Celý popis

Uložené v:

Podrobná bibliografia
Vydané v:	Frontiers in endocrinology (Lausanne) Ročník 13; s. 935106
Hlavní autori:	Kuehnemann, Chisaka, Hu, Kang-Quan, Butera, Kayla, Patel, Sandip K., Bons, Joanna, Schilling, Birgit, Aguayo-Mazzucato, Cristina, Wiley, Christopher D.
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	Switzerland Frontiers Media S.A 14.07.2022
Predmet:	AMP-Activated Protein Kinases - metabolism Animals cellular senescence Cytokines - genetics Cytokines - metabolism Diabetes Mellitus, Experimental - metabolism eNAMPT Endocrinology Mice NAD NAD - metabolism NAMPT Nicotinamide Phosphoribosyltransferase - genetics Nicotinamide Phosphoribosyltransferase - metabolism SASP senescence Senescence-Associated Secretory Phenotype - genetics Senescence-Associated Secretory Phenotype - physiology NAD senescence cellular senescence NAMPT eNAMPT aging SASP diabetes
ISSN:	1664-2392, 1664-2392
On-line prístup:	Získať plný text
Tagy:	Pridať tag Žiadne tagy, Buďte prvý, kto otaguje tento záznam!

Abstract	Cellular senescence is a stress or damage response by which a cell adopts of state of essentially permanent proliferative arrest, coupled to the secretion of a number of biologically active molecules. This senescence-associated secretory phenotype (SASP) underlies many of the degenerative and regenerative aspects of cellular senescence - including promoting wound healing and development, but also driving diabetes and multiple age-associated diseases. We find that nicotinamide phosphoribosyltransferase (NAMPT), which catalyzes the rate-limiting step in nicotinamide adenine dinucleotide (NAD) biosynthesis, is elevated in senescent cells without a commensurate increase in NAD levels. This elevation is distinct from the acute DNA damage response, in which NAD is depleted, and recovery of NAD by NAMPT elevation is AMPK-activated protein kinase (AMPK)-dependent. Instead, we find that senescent cells release extracellular NAMPT (eNAMPT) as part of the SASP. eNAMPT has been reported to be released as a catalytically active extracellular vesicle-contained dimer that promotes NAD increases in other cells and extends lifespan, and also as free monomer that acts as a damage-associated molecular pattern and promotes conditions such as diabetes and fibrosis. Senescent cells released eNAMPT as dimer, but surprisingly eNAMPT appeared in the soluble secretome while being depleted from exosomes. Finally, diabetic mice showed elevated levels of eNAMPT, and this was lowered by treatment with the senolytic drug, ABT-263. Together, these data reveal a new SASP factor with implications for NAD metabolism.
AbstractList	Cellular senescence is a stress or damage response by which a cell adopts of state of essentially permanent proliferative arrest, coupled to the secretion of a number of biologically active molecules. This senescence-associated secretory phenotype (SASP) underlies many of the degenerative and regenerative aspects of cellular senescence - including promoting wound healing and development, but also driving diabetes and multiple age-associated diseases. We find that nicotinamide phosphoribosyltransferase (NAMPT), which catalyzes the rate-limiting step in nicotinamide adenine dinucleotide (NAD) biosynthesis, is elevated in senescent cells without a commensurate increase in NAD levels. This elevation is distinct from the acute DNA damage response, in which NAD is depleted, and recovery of NAD by NAMPT elevation is AMPK-activated protein kinase (AMPK)-dependent. Instead, we find that senescent cells release extracellular NAMPT (eNAMPT) as part of the SASP. eNAMPT has been reported to be released as a catalytically active extracellular vesicle-contained dimer that promotes NAD increases in other cells and extends lifespan, and also as free monomer that acts as a damage-associated molecular pattern and promotes conditions such as diabetes and fibrosis. Senescent cells released eNAMPT as dimer, but surprisingly eNAMPT appeared in the soluble secretome while being depleted from exosomes. Finally, diabetic mice showed elevated levels of eNAMPT, and this was lowered by treatment with the senolytic drug, ABT-263. Together, these data reveal a new SASP factor with implications for NAD metabolism.Cellular senescence is a stress or damage response by which a cell adopts of state of essentially permanent proliferative arrest, coupled to the secretion of a number of biologically active molecules. This senescence-associated secretory phenotype (SASP) underlies many of the degenerative and regenerative aspects of cellular senescence - including promoting wound healing and development, but also driving diabetes and multiple age-associated diseases. We find that nicotinamide phosphoribosyltransferase (NAMPT), which catalyzes the rate-limiting step in nicotinamide adenine dinucleotide (NAD) biosynthesis, is elevated in senescent cells without a commensurate increase in NAD levels. This elevation is distinct from the acute DNA damage response, in which NAD is depleted, and recovery of NAD by NAMPT elevation is AMPK-activated protein kinase (AMPK)-dependent. Instead, we find that senescent cells release extracellular NAMPT (eNAMPT) as part of the SASP. eNAMPT has been reported to be released as a catalytically active extracellular vesicle-contained dimer that promotes NAD increases in other cells and extends lifespan, and also as free monomer that acts as a damage-associated molecular pattern and promotes conditions such as diabetes and fibrosis. Senescent cells released eNAMPT as dimer, but surprisingly eNAMPT appeared in the soluble secretome while being depleted from exosomes. Finally, diabetic mice showed elevated levels of eNAMPT, and this was lowered by treatment with the senolytic drug, ABT-263. Together, these data reveal a new SASP factor with implications for NAD metabolism. Cellular senescence is a stress or damage response by which a cell adopts of state of essentially permanent proliferative arrest, coupled to the secretion of a number of biologically active molecules. This senescence-associated secretory phenotype (SASP) underlies many of the degenerative and regenerative aspects of cellular senescence - including promoting wound healing and development, but also driving diabetes and multiple age-associated diseases. We find that nicotinamide phosphoribosyltransferase (NAMPT), which catalyzes the rate-limiting step in nicotinamide adenine dinucleotide (NAD) biosynthesis, is elevated in senescent cells without a commensurate increase in NAD levels. This elevation is distinct from the acute DNA damage response, in which NAD is depleted, and recovery of NAD by NAMPT elevation is AMPK-activated protein kinase (AMPK)-dependent. Instead, we find that senescent cells release extracellular NAMPT (eNAMPT) as part of the SASP. eNAMPT has been reported to be released as a catalytically active extracellular vesicle-contained dimer that promotes NAD increases in other cells and extends lifespan, and also as free monomer that acts as a damage-associated molecular pattern and promotes conditions such as diabetes and fibrosis. Senescent cells released eNAMPT as dimer, but surprisingly eNAMPT appeared in the soluble secretome while being depleted from exosomes. Finally, diabetic mice showed elevated levels of eNAMPT, and this was lowered by treatment with the senolytic drug, ABT-263. Together, these data reveal a new SASP factor with implications for NAD metabolism.
Author	Aguayo-Mazzucato, Cristina Bons, Joanna Schilling, Birgit Hu, Kang-Quan Wiley, Christopher D. Butera, Kayla Patel, Sandip K. Kuehnemann, Chisaka
AuthorAffiliation	3 Joslin Diabetes Center, Harvard Medical School , Boston, MA , United States 1 Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University , Boston, MA , United States 2 Buck Institute for Research on Aging , Novato, CA , United States
AuthorAffiliation_xml	– name: 1 Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University , Boston, MA , United States – name: 3 Joslin Diabetes Center, Harvard Medical School , Boston, MA , United States – name: 2 Buck Institute for Research on Aging , Novato, CA , United States
Author_xml	– sequence: 1 givenname: Chisaka surname: Kuehnemann fullname: Kuehnemann, Chisaka – sequence: 2 givenname: Kang-Quan surname: Hu fullname: Hu, Kang-Quan – sequence: 3 givenname: Kayla surname: Butera fullname: Butera, Kayla – sequence: 4 givenname: Sandip K. surname: Patel fullname: Patel, Sandip K. – sequence: 5 givenname: Joanna surname: Bons fullname: Bons, Joanna – sequence: 6 givenname: Birgit surname: Schilling fullname: Schilling, Birgit – sequence: 7 givenname: Cristina surname: Aguayo-Mazzucato fullname: Aguayo-Mazzucato, Cristina – sequence: 8 givenname: Christopher D. surname: Wiley fullname: Wiley, Christopher D.
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/35909566$$D View this record in MEDLINE/PubMed
BookMark	eNp1kk1v1DAQhi1UREvpD-CCcuSyi78TX5CqVYGVKkACzpZjT7quEjvYXsT-e5xui1okfPFo_M4ztud9iU5CDIDQa4LXjHXq3QDBxTXFlK4VEwTLZ-iMSMlXlCl68ig-RRc53-K6OCZKdS_QKRMKKyHlGSpXv0syFsZxP5rUfPY2Fh_M5B00X3cxz7uYfB_zYayykAdIJkOzzY1pNnGa65VCaeLQlB003yBAthAsrC5zjtabAq5mbYIS06HyIMRymOEVej6YMcPF_X6Ofny4-r75tLr-8nG7ubxeWS5FWQluJccOEykwJZxby2HgjrtWWMerhFgAkLwTYETftcBYjy0XeGAcA8HsHG2PXBfNrZ6Tn0w66Gi8vkvEdKNNKt6OoDFmHRWGUNU7PrSiVzVShHcWTEeBVNb7I2ve9xO4-sz6IeMT6NOT4Hf6Jv7SilEl6AJ4ew9I8ecectGTz8vHmwBxnzWVqq1DIbir0jePe_1t8jC2KmiPAptizgkGbX0xxceltR81wXrxiL7ziF48oo8eqZXkn8oH-P9r_gA2qcJ4
CitedBy_id	crossref_primary_10_2147_DMSO_S543814 crossref_primary_10_1038_s41420_025_02672_w crossref_primary_10_1016_j_biopha_2024_116962 crossref_primary_10_1186_s12943_024_02096_7 crossref_primary_10_1016_j_ejcb_2024_151438 crossref_primary_10_1186_s40001_023_01604_7 crossref_primary_10_3389_fimmu_2023_1268756 crossref_primary_10_1111_acel_13920
Cites_doi	10.1007/s11357-016-9954-6 10.1016/j.cmet.2015.11.011 10.1152/ajpheart.00468.2012 10.1183/13993003.02536-2020 10.1016/j.isci.2022.104147 10.1074/mcp.RA117.000314 10.1002/cpz1.32 10.1038/nm.4010 10.1182/blood-2014-07-589069 10.1111/acel.12632 10.1007/s00125-019-05029-y 10.1038/s42255-020-00305-3 10.1021/acs.jproteome.7b00170 10.1111/acel.12950 10.1038/s42255-020-00298-z 10.1016/j.cmet.2011.08.014 10.1101/cshperspect.a025163 10.1074/jbc.M805866200 10.1016/j.cmet.2019.05.015 10.1101/2021.02.27.433188 10.1016/j.cell.2013.11.037 10.1016/j.cmet.2019.05.006 10.1038/srep13135 10.1002/pmic.201100463 10.3389/fendo.2017.00196 10.1038/s41556-019-0287-4 10.1073/pnas.93.19.10309 10.1007/s00125-006-0173-z 10.1016/j.devcel.2014.11.012 10.1371/journal.pbio.0060301 10.1007/s00109-020-01892-0 10.1016/j.cmet.2015.04.002 10.1165/rcmb.2021-0357OC 10.1371/journal.pone.0047978 10.1016/j.cmet.2016.05.006 10.1016/j.bbrc.2009.11.066 10.1172/JCI13505 10.1073/pnas.92.20.9363 10.1016/j.ijrobp.2017.02.216 10.1083/jcb.201206006 10.1038/s41598-018-20000-4 10.1016/j.cell.2013.10.041 10.1007/s00125-016-4076-3 10.1038/nature16932 10.1126/science.aaf2693 10.18632/oncotarget.24871 10.1371/journal.pbio.3000599 10.1073/pnas.1417921112 10.1016/j.cmet.2019.01.021 10.1126/sciadv.abj9109 10.1172/jci.insight.130056 10.1038/s42255-021-00483-8 10.1016/j.cell.2013.10.019 10.1523/JNEUROSCI.4730-13.2014 10.1038/ncomms14532
ContentType	Journal Article
Copyright	Copyright © 2022 Kuehnemann, Hu, Butera, Patel, Bons, Schilling, Aguayo-Mazzucato and Wiley. Copyright © 2022 Kuehnemann, Hu, Butera, Patel, Bons, Schilling, Aguayo-Mazzucato and Wiley 2022 Kuehnemann, Hu, Butera, Patel, Bons, Schilling, Aguayo-Mazzucato and Wiley
Copyright_xml	– notice: Copyright © 2022 Kuehnemann, Hu, Butera, Patel, Bons, Schilling, Aguayo-Mazzucato and Wiley. – notice: Copyright © 2022 Kuehnemann, Hu, Butera, Patel, Bons, Schilling, Aguayo-Mazzucato and Wiley 2022 Kuehnemann, Hu, Butera, Patel, Bons, Schilling, Aguayo-Mazzucato and Wiley
DBID	AAYXX CITATION CGR CUY CVF ECM EIF NPM 7X8 5PM DOA
DOI	10.3389/fendo.2022.935106
DatabaseName	CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed 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) MEDLINE - Academic
DatabaseTitleList	MEDLINE - Academic MEDLINE CrossRef
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: 7X8 name: MEDLINE - Academic url: https://search.proquest.com/medline sourceTypes: Aggregation Database
DeliveryMethod	fulltext_linktorsrc
Discipline	Medicine
EISSN	1664-2392
ExternalDocumentID	oai_doaj_org_article_003825a129bd4f75b929b9148cea82e1 PMC9329521 35909566 10_3389_fendo_2022_935106
Genre	Journal Article
GrantInformation_xml	– fundername: NIDDK NIH HHS grantid: R01 DK132535 – fundername: NIH HHS grantid: S10 OD028654 – fundername: NIA NIH HHS grantid: P01 AG017242 – fundername: NIA NIH HHS grantid: U01 AG060906 – fundername: ; – fundername: ; grantid: AG017242
GroupedDBID	53G 5VS 9T4 AAFWJ AAKDD AAYXX ACGFO ACGFS ADBBV ADRAZ AFPKN ALMA_UNASSIGNED_HOLDINGS AOIJS BAWUL BCNDV CITATION DIK EMOBN GROUPED_DOAJ GX1 HYE KQ8 M48 M~E OK1 PGMZT RPM CGR CUY CVF ECM EIF IPNFZ NPM RIG 7X8 5PM
ID	FETCH-LOGICAL-c465t-54c640d016502144cc4ef4d4d75cd44651ceee6485ea5b87e33b0c450f340e103
IEDL.DBID	DOA
ISICitedReferencesCount	11
ISICitedReferencesURI	http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000833825300001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN	1664-2392
IngestDate	Fri Oct 03 12:52:56 EDT 2025 Thu Aug 21 18:23:04 EDT 2025 Fri Sep 05 12:44:23 EDT 2025 Sat Nov 01 14:15:56 EDT 2025 Tue Nov 18 22:12:43 EST 2025 Sat Nov 29 06:38:31 EST 2025
IsDoiOpenAccess	true
IsOpenAccess	true
IsPeerReviewed	true
IsScholarly	true
Keywords	NAD senescence cellular senescence NAMPT eNAMPT aging SASP diabetes
Language	English
License	Copyright © 2022 Kuehnemann, Hu, Butera, Patel, Bons, Schilling, Aguayo-Mazzucato and Wiley. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
LinkModel	DirectLink
MergedId	FETCHMERGED-LOGICAL-c465t-54c640d016502144cc4ef4d4d75cd44651ceee6485ea5b87e33b0c450f340e103
Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Edited by: Luigi Ferrucci, National Institute on Aging (NIH), United States Reviewed by: Brenna Osborne, University of Copenhagen, Denmark; Bela Ozsvari, University of Salford, United Kingdom This article was submitted to Endocrinology of Aging, a section of the journal Frontiers in Endocrinology
OpenAccessLink	https://doaj.org/article/003825a129bd4f75b929b9148cea82e1
PMID	35909566
PQID	2697095108
PQPubID	23479
ParticipantIDs	doaj_primary_oai_doaj_org_article_003825a129bd4f75b929b9148cea82e1 pubmedcentral_primary_oai_pubmedcentral_nih_gov_9329521 proquest_miscellaneous_2697095108 pubmed_primary_35909566 crossref_citationtrail_10_3389_fendo_2022_935106 crossref_primary_10_3389_fendo_2022_935106
PublicationCentury	2000
PublicationDate	2022-07-14
PublicationDateYYYYMMDD	2022-07-14
PublicationDate_xml	– month: 07 year: 2022 text: 2022-07-14 day: 14
PublicationDecade	2020
PublicationPlace	Switzerland
PublicationPlace_xml	– name: Switzerland
PublicationTitle	Frontiers in endocrinology (Lausanne)
PublicationTitleAlternate	Front Endocrinol (Lausanne)
PublicationYear	2022
Publisher	Frontiers Media S.A
Publisher_xml	– name: Frontiers Media S.A
References	Demaria (B16) 2014; 31 Yoshida (B22) 2019; 30 Chang (B14) 2016; 22 Neri (B42) 2021; 1 Zhu (B4) 2015; 112 Wiley (B9) 2019; 4 Aguayo-Mazzucato (B8) 2019; 30 Coppe (B41) 2008; 6 Ethier (B48) 2012; 7 Chini (B39) 2020; 2 Sayers (B35) 2020; 63 Schafer (B11) 2017; 8 Morato (B28) 2022; 8 Colombo (B56) 2020; 98 Colombo (B32) 2022; 25 Yoon (B29) 2015; 21 Li (B30) 2008; 283 Pillai (B27) 2013; 304 Storer (B18) 2013; 155 Ben-Hur (B47) 1984; 6 Covarrubias (B38) 2020; 2 Nacarelli (B37) 2019; 21 Wiley (B40) 2017; 16 Ossovskaya (B52) 1996; 93 Quijada (B55) 2021; 57 Baker (B6) 2016; 530 Thompson (B12) 2019; 29 Bruderer (B45) 2017; 16 Zhou (B49) 2001; 108 Zhang (B7) 2016; 352 Palmer (B10) 2019; 18 Burger (B46) 2018; 17 Basisty (B54) 2020; 18 Sierra (B1) 2017; 39 Sierra (B2) 2016; 6 Audrito (B31) 2015; 125 Patel (B43) 2021; 27 Munoz-Espin (B17) 2013; 155 Menon (B19) 2017; 8 Escher (B44) 2012; 12 Davalos (B51) 2013; 201 Wiley (B50) 2018; 8 Wiley (B36) 2016; 23 Camp (B53) 2015; 5 Pan (B15) 2017; 99 Wiley (B13) 2021; 3 Curat (B25) 2006; 49 Stein (B23) 2014; 34 Garten (B24) 2010; 391 Yoshino (B21) 2011; 14 Audrito (B26) 2018; 9 Kieswich (B34) 2016; 59 Dimri (B5) 1995; 92 Gomes (B3) 2013; 155 Camacho-Pereira (B20) 2016; 23 Garcia (B33) 2022; 66
References_xml	– volume: 39 start-page: 1 year: 2017 ident: B1 article-title: Geroscience and the Trans-NIH Geroscience Interest Group, GSIG publication-title: Geroscience doi: 10.1007/s11357-016-9954-6 – volume: 23 year: 2016 ident: B36 article-title: Mitochondrial Dysfunction Induces Senescence With a Distinct Secretory Phenotype publication-title: Cell Metab doi: 10.1016/j.cmet.2015.11.011 – volume: 304 year: 2013 ident: B27 article-title: Nampt Secreted From Cardiomyocytes Promotes Development of Cardiac Hypertrophy and Adverse Ventricular Remodeling publication-title: Am J Physiol Heart Circ Physiol doi: 10.1152/ajpheart.00468.2012 – volume: 57 year: 2021 ident: B55 article-title: Endothelial eNAMPT Amplifies Pre-Clinical Acute Lung Injury: Efficacy of an eNAMPT-Neutralising Monoclonal Antibody publication-title: Eur Respir J doi: 10.1183/13993003.02536-2020 – volume: 25 start-page: 104147 year: 2022 ident: B32 article-title: Extracellular Nicotinamide Phosphoribosyltransferase Boosts IFNgamma-Induced Macrophage Polarization Independently of TLR4 publication-title: iScience doi: 10.1016/j.isci.2022.104147 – volume: 16 year: 2017 ident: B45 article-title: Optimization of Experimental Parameters in Data-Independent Mass Spectrometry Significantly Increases Depth and Reproducibility of Results publication-title: Mol Cell Proteomics doi: 10.1074/mcp.RA117.000314 – volume: 1 start-page: e32 year: 2021 ident: B42 article-title: Quantitative Proteomic Analysis of the Senescence-Associated Secretory Phenotype by Data-Independent Acquisition publication-title: Curr Protoc doi: 10.1002/cpz1.32 – volume: 22 start-page: 78 year: 2016 ident: B14 article-title: Clearance of Senescent Cells by ABT263 Rejuvenates Aged Hematopoietic Stem Cells in Mice publication-title: Nat Med doi: 10.1038/nm.4010 – volume: 125 year: 2015 ident: B31 article-title: Extracellular Nicotinamide Phosphoribosyltransferase (NAMPT) Promotes M2 Macrophage Polarization in Chronic Lymphocytic Leukemia publication-title: Blood doi: 10.1182/blood-2014-07-589069 – volume: 16 year: 2017 ident: B40 article-title: Analysis of Individual Cells Identifies Cell-to-Cell Variability Following Induction of Cellular Senescence publication-title: Aging Cell doi: 10.1111/acel.12632 – volume: 63 year: 2020 ident: B35 article-title: Structure-Functional Changes in eNAMPT at High Concentrations Mediate Mouse and Human Beta Cell Dysfunction in Type 2 Diabetes publication-title: Diabetologia doi: 10.1007/s00125-019-05029-y – volume: 2 year: 2020 ident: B38 article-title: Senescent Cells Promote Tissue NAD(+) Decline During Ageing via the Activation of CD38(+) Macrophages publication-title: Nat Metab doi: 10.1038/s42255-020-00305-3 – volume: 17 start-page: 12 year: 2018 ident: B46 article-title: Gentle Introduction to the Statistical Foundations of False Discovery Rate in Quantitative Proteomics publication-title: J Proteome Res doi: 10.1021/acs.jproteome.7b00170 – volume: 18 year: 2019 ident: B10 article-title: Targeting Senescent Cells Alleviates Obesity-Induced Metabolic Dysfunction publication-title: Aging Cell doi: 10.1111/acel.12950 – volume: 2 year: 2020 ident: B39 article-title: CD38 Ecto-Enzyme in Immune Cells is Induced During Aging and Regulates NAD(+) and NMN Levels publication-title: Nat Metab doi: 10.1038/s42255-020-00298-z – volume: 14 year: 2011 ident: B21 article-title: Nicotinamide Mononucleotide, a Key NAD(+) Intermediate, Treats the Pathophysiology of Diet- and Age-Induced Diabetes in Mice publication-title: Cell Metab doi: 10.1016/j.cmet.2011.08.014 – volume: 6 start-page: a025163 year: 2016 ident: B2 article-title: The Emergence of Geroscience as an Interdisciplinary Approach to the Enhancement of Health Span and Life Span publication-title: Cold Spring Harb Perspect Med doi: 10.1101/cshperspect.a025163 – volume: 283 year: 2008 ident: B30 article-title: Extracellular Nampt Promotes Macrophage Survival via a Nonenzymatic Interleukin-6/STAT3 Signaling Mechanism publication-title: J Biol Chem doi: 10.1074/jbc.M805866200 – volume: 30 start-page: 329 year: 2019 ident: B22 article-title: Extracellular Vesicle-Contained eNAMPT Delays Aging and Extends Lifespan in Mice publication-title: Cell Metab doi: 10.1016/j.cmet.2019.05.015 – volume: 27 start-page: 433188 year: 2021 ident: B43 article-title: Comprehensive Profiling of Plasma Exosomes Using Data-Independent Acquisitions – New Tools for Aging Cohort Studies publication-title: bioRxiv doi: 10.1101/2021.02.27.433188 – volume: 155 year: 2013 ident: B3 article-title: Declining NAD(+) Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication During Aging publication-title: Cell doi: 10.1016/j.cell.2013.11.037 – volume: 30 start-page: 129 year: 2019 ident: B8 article-title: Acceleration of Beta Cell Aging Determines Diabetes and Senolysis Improves Disease Outcomes publication-title: Cell Metab doi: 10.1016/j.cmet.2019.05.006 – volume: 5 start-page: 13135 year: 2015 ident: B53 article-title: Unique Toll-Like Receptor 4 Activation by NAMPT/PBEF Induces NFkappaB Signaling and Inflammatory Lung Injury publication-title: Sci Rep doi: 10.1038/srep13135 – volume: 12 year: 2012 ident: B44 article-title: Using iRT, a Normalized Retention Time for More Targeted Measurement of Peptides publication-title: Proteomics doi: 10.1002/pmic.201100463 – volume: 8 year: 2017 ident: B19 article-title: Programmed Fetal Membrane Senescence and Exosome-Mediated Signaling: A Mechanism Associated With Timing of Human Parturition publication-title: Front Endocrinol (Lausanne) doi: 10.3389/fendo.2017.00196 – volume: 21 start-page: 397 year: 2019 ident: B37 article-title: NAD(+) Metabolism Governs the Proinflammatory Senescence-Associated Secretome publication-title: Nat Cell Biol doi: 10.1038/s41556-019-0287-4 – volume: 93 year: 1996 ident: B52 article-title: Use of Genetic Suppressor Elements to Dissect Distinct Biological Effects of Separate P53 Domains publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.93.19.10309 – volume: 49 year: 2006 ident: B25 article-title: Macrophages in Human Visceral Adipose Tissue: Increased Accumulation in Obesity and a Source of Resistin and Visfatin publication-title: Diabetologia doi: 10.1007/s00125-006-0173-z – volume: 31 year: 2014 ident: B16 article-title: An Essential Role for Senescent Cells in Optimal Wound Healing Through Secretion of PDGF-Aa publication-title: Dev Cell doi: 10.1016/j.devcel.2014.11.012 – volume: 6 year: 2008 ident: B41 article-title: Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the P53 Tumor Suppressor publication-title: PloS Biol doi: 10.1371/journal.pbio.0060301 – volume: 98 start-page: 595 year: 2020 ident: B56 article-title: Neutralization of Extracellular NAMPT (Nicotinamide Phosphoribosyltransferase) Ameliorates Experimental Murine Colitis publication-title: J Mol Med (Berl) doi: 10.1007/s00109-020-01892-0 – volume: 21 year: 2015 ident: B29 article-title: SIRT1-Mediated eNAMPT Secretion From Adipose Tissue Regulates Hypothalamic NAD+ and Function in Mice publication-title: Cell Metab doi: 10.1016/j.cmet.2015.04.002 – volume: 66 year: 2022 ident: B33 article-title: eNAMPT is a Novel DAMP That Contributes to the Severity of Radiation-Induced Lung Fibrosis publication-title: Am J Respir Cell Mol Biol doi: 10.1165/rcmb.2021-0357OC – volume: 7 year: 2012 ident: B48 article-title: PARP-1 Modulation of mTOR Signaling in Response to a DNA Alkylating Agent publication-title: PloS One doi: 10.1371/journal.pone.0047978 – volume: 23 year: 2016 ident: B20 article-title: CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction Through an SIRT3-Dependent Mechanism publication-title: Cell Metab doi: 10.1016/j.cmet.2016.05.006 – volume: 391 year: 2010 ident: B24 article-title: Nicotinamide Phosphoribosyltransferase (NAMPT/PBEF/visfatin) Is Constitutively Released From Human Hepatocytes publication-title: Biochem Biophys Res Commun doi: 10.1016/j.bbrc.2009.11.066 – volume: 108 year: 2001 ident: B49 article-title: Role of AMP-Activated Protein Kinase in Mechanism of Metformin Action publication-title: J Clin Invest doi: 10.1172/JCI13505 – volume: 92 year: 1995 ident: B5 article-title: A Biomarker That Identifies Senescent Human Cells in Culture and in Aging Skin In Vivo publication-title: Proc Natl Acad Sci U.S.A. doi: 10.1073/pnas.92.20.9363 – volume: 99 year: 2017 ident: B15 article-title: Inhibition of Bcl-2/Xl With ABT-263 Selectively Kills Senescent Type II Pneumocytes and Reverses Persistent Pulmonary Fibrosis Induced by Ionizing Radiation in Mice publication-title: Int J Radiat Oncol Biol Phys doi: 10.1016/j.ijrobp.2017.02.216 – volume: 201 year: 2013 ident: B51 article-title: P53-Dependent Release of Alarmin HMGB1 Is a Central Mediator of Senescent Phenotypes publication-title: J Cell Biol doi: 10.1083/jcb.201206006 – volume: 8 start-page: 2410 year: 2018 ident: B50 article-title: Small-Molecule MDM2 Antagonists Attenuate the Senescence-Associated Secretory Phenotype publication-title: Sci Rep doi: 10.1038/s41598-018-20000-4 – volume: 155 year: 2013 ident: B18 article-title: Senescence Is a Developmental Mechanism That Contributes to Embryonic Growth and Patterning publication-title: Cell doi: 10.1016/j.cell.2013.10.041 – volume: 59 year: 2016 ident: B34 article-title: Monomeric eNAMPT in the Development of Experimental Diabetes in Mice: A Potential Target for Type 2 Diabetes Treatment publication-title: Diabetologia doi: 10.1007/s00125-016-4076-3 – volume: 6 start-page: 39 year: 1984 ident: B47 article-title: Inhibitors of Poly (ADP-Ribose) Synthesis Enhance Radiation Response by Differentially Affecting Repair of Potentially Lethal Versus Sublethal Damage publication-title: Br J Cancer Suppl – volume: 530 year: 2016 ident: B6 article-title: Naturally Occurring P16(Ink4a)-Positive Cells Shorten Healthy Lifespan publication-title: Nature doi: 10.1038/nature16932 – volume: 352 year: 2016 ident: B7 article-title: NAD(+) Repletion Improves Mitochondrial and Stem Cell Function and Enhances Life Span in Mice publication-title: Science doi: 10.1126/science.aaf2693 – volume: 9 year: 2018 ident: B26 article-title: Extracellular Nicotinamide Phosphoribosyltransferase (eNAMPT) is a Novel Marker for Patients With BRAF-Mutated Metastatic Melanoma publication-title: Oncotarget doi: 10.18632/oncotarget.24871 – volume: 18 year: 2020 ident: B54 article-title: A Proteomic Atlas of Senescence-Associated Secretomes for Aging Biomarker Development publication-title: PloS Biol doi: 10.1371/journal.pbio.3000599 – volume: 112 year: 2015 ident: B4 article-title: In Vivo NAD Assay Reveals the Intracellular NAD Contents and Redox State in Healthy Human Brain and Their Age Dependences publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.1417921112 – volume: 29 start-page: 1045 year: 2019 ident: B12 article-title: Targeted Elimination of Senescent Beta Cells Prevents Type 1 Diabetes publication-title: Cell Metab doi: 10.1016/j.cmet.2019.01.021 – volume: 8 year: 2022 ident: B28 article-title: eNAMPT Actions Through Nucleus Accumbens NAD(+)/SIRT1 Link Increased Adiposity With Sociability Deficits Programmed by Peripuberty Stress publication-title: Sci Adv doi: 10.1126/sciadv.abj9109 – volume: 4 year: 2019 ident: B9 article-title: Secretion of Leukotrienes by Senescent Lung Fibroblasts Promotes Pulmonary Fibrosis publication-title: JCI Insight doi: 10.1172/jci.insight.130056 – volume: 3 year: 2021 ident: B13 article-title: The Metabolic Roots of Senescence: Mechanisms and Opportunities for Intervention publication-title: Nat Metab doi: 10.1038/s42255-021-00483-8 – volume: 155 year: 2013 ident: B17 article-title: Programmed Cell Senescence During Mammalian Embryonic Development publication-title: Cell doi: 10.1016/j.cell.2013.10.019 – volume: 34 year: 2014 ident: B23 article-title: Expression of Nampt in Hippocampal and Cortical Excitatory Neurons is Critical for Cognitive Function publication-title: J Neurosci doi: 10.1523/JNEUROSCI.4730-13.2014 – volume: 8 start-page: 14532 year: 2017 ident: B11 article-title: Cellular Senescence Mediates Fibrotic Pulmonary Disease publication-title: Nat Commun doi: 10.1038/ncomms14532
SSID	ssj0000401998
Score	2.3554797
Snippet	Cellular senescence is a stress or damage response by which a cell adopts of state of essentially permanent proliferative arrest, coupled to the secretion of a...
SourceID	doaj pubmedcentral proquest pubmed crossref
SourceType	Open Website Open Access Repository Aggregation Database Index Database Enrichment Source
StartPage	935106
SubjectTerms	AMP-Activated Protein Kinases - metabolism Animals cellular senescence Cytokines - genetics Cytokines - metabolism Diabetes Mellitus, Experimental - metabolism eNAMPT Endocrinology Mice NAD NAD - metabolism NAMPT Nicotinamide Phosphoribosyltransferase - genetics Nicotinamide Phosphoribosyltransferase - metabolism SASP senescence Senescence-Associated Secretory Phenotype - genetics Senescence-Associated Secretory Phenotype - physiology
Title	Extracellular Nicotinamide Phosphoribosyltransferase Is a Component of the Senescence-Associated Secretory Phenotype
URI	https://www.ncbi.nlm.nih.gov/pubmed/35909566 https://www.proquest.com/docview/2697095108 https://pubmed.ncbi.nlm.nih.gov/PMC9329521 https://doaj.org/article/003825a129bd4f75b929b9148cea82e1
Volume	13
WOSCitedRecordID	wos000833825300001&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: PRVAON databaseName: DOAJ Directory of Open Access Journals customDbUrl: eissn: 1664-2392 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0000401998 issn: 1664-2392 databaseCode: DOA dateStart: 20100101 isFulltext: true titleUrlDefault: https://www.doaj.org/ providerName: Directory of Open Access Journals – providerCode: PRVHPJ databaseName: ROAD: Directory of Open Access Scholarly Resources customDbUrl: eissn: 1664-2392 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0000401998 issn: 1664-2392 databaseCode: M~E dateStart: 20100101 isFulltext: true titleUrlDefault: https://road.issn.org providerName: ISSN International Centre
link	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lb9QwELZKVSEuCCjQ5VEZqSekQDaxk_gI1VZwaFWJVtqb5Ve0K1VJtUkRXPjtfONkV7sIlQuXHBLbGfkbe77xY4axE-elqMHDE5WVcFCECYnxwWMyhNhWwWJYEZNNlBcX1XyuLrdSfdGZsCE88NBxlGwMToyBWbIerUoLe442ROWCqbIQHR-wni1nKs7BcBvgSAzbmPDC1Mc6NJ4u-2XZB5VDEYsdQxTj9f-NZP55VnLL-Jw9YY9H1sg_DdI-ZXuhecYeno_74oesn_1ANVqEp1OlnODtl5Rq3gd-uWi720W7Wtq2-3nTR6IaVjBe_GvHDacJoW3wW97WHGyQf6PZz9GAT9bYBY-3oJe0IY_2QtPSyu1zdn02uzr9koz5FBInCtknUrhCpJ4uMMVIac6JUAsvfCmdp8BpU1jMUIhKBiNtVYY8t6kTMq1zkYZpmr9g-w0kOmLcVAqFpnRt1wmQAOWdVb40aM2CAMoJS9edq90YbJxyXtxoOB2Eh454aMJDD3hM2PtNldsh0sZ9hT8TYpuCFCQ7voDq6FF19L9UZ8LerfHWGFQEkmlCe9fprFBl5J7VhL0c8N_8KpeKgjdChHJHM3Zk2f3SLBcxcDe4sgJdevU_hH_NHlF_0DLzVLxh-_3qLrxlB-57v-xWx-xBOa-O45jA8_zX7Dd1ABOK
linkProvider	Directory of Open Access Journals
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=Extracellular+Nicotinamide+Phosphoribosyltransferase+Is+a+Component+of+the+Senescence-Associated+Secretory+Phenotype&rft.jtitle=Frontiers+in+endocrinology+%28Lausanne%29&rft.au=Kuehnemann%2C+Chisaka&rft.au=Hu%2C+Kang-Quan&rft.au=Butera%2C+Kayla&rft.au=Patel%2C+Sandip+K&rft.date=2022-07-14&rft.issn=1664-2392&rft.eissn=1664-2392&rft.volume=13&rft.spage=935106&rft_id=info:doi/10.3389%2Ffendo.2022.935106&rft.externalDBID=NO_FULL_TEXT
thumbnail_l	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1664-2392&client=summon
thumbnail_m	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1664-2392&client=summon
thumbnail_s	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1664-2392&client=summon