Circulating N-formylmethionine and metabolic shift in critical illness: a multicohort metabolomics study

Background Cell stress promotes degradation of mitochondria which release danger-associated molecular patterns that are catabolized to N -formylmethionine. We hypothesized that in critically ill adults, the response to N -formylmethionine is associated with increases in metabolomic shift-related met...

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Veröffentlicht in:	Critical Care Jg. 26; H. 1; S. 321 - 13
Hauptverfasser:	Sigurdsson, Martin Ingi, Kobayashi, Hirotada, Amrein, Karin, Nakahira, Kiichi, Rogers, Angela J., Pinilla-Vera, Mayra, Baron, Rebecca M., Fredenburgh, Laura E., Lasky-Su, Jessica A., Christopher, Kenneth B.
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	London Springer Science and Business Media LLC 19.10.2022 BioMed Central BioMed Central Ltd BMC
Schlagworte:	Acylcarnitine Adult Amino Acids, Branched-Chain Care and treatment Clinical Trials as Topic Critical Care Medicine Critical Illness Critically ill Emergency Medicine Fatty Acids Female Health aspects Hospital Mortality Humans Intensive Intensive Care Units Kynurenine Medical emergencies. Critical care. Intensive care. First aid Medicine Medicine & Public Health Metabolic shift Metabolomics Metabolomics - methods Methionine N-Formylmethionine Pentose phosphate pathway Prognosis RC86-88.9 Metabolic shift Metabolomics Critical illness Branched chain amino acids formylmethionine Acylcarnitine Pentose phosphate pathway N-formylmethionine
ISSN:	1364-8535, 1466-609X, 1364-8535, 1466-609X
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Abstract	Background Cell stress promotes degradation of mitochondria which release danger-associated molecular patterns that are catabolized to N -formylmethionine. We hypothesized that in critically ill adults, the response to N -formylmethionine is associated with increases in metabolomic shift-related metabolites and increases in 28-day mortality. Methods We performed metabolomics analyses on plasma from the 428-subject Correction of Vitamin D Deficiency in Critically Ill Patients trial (VITdAL-ICU) cohort and the 90-subject Brigham and Women’s Hospital Registry of Critical Illness (RoCI) cohort. In the VITdAL-ICU cohort, we analyzed 983 metabolites at Intensive Care Unit (ICU) admission, day 3, and 7. In the RoCI cohort, we analyzed 411 metabolites at ICU admission. The association between N -formylmethionine and mortality was determined by adjusted logistic regression. The relationship between individual metabolites and N -formylmethionine abundance was assessed with false discovery rate correction via linear regression, linear mixed-effects, and Gaussian graphical models. Results Patients with the top quartile of N -formylmethionine abundance at ICU admission had a significantly higher adjusted odds of 28-day mortality in the VITdAL-ICU (OR, 2.4; 95%CI 1.5–4.0; P = 0.001) and RoCI cohorts (OR, 5.1; 95%CI 1.4–18.7; P = 0.015). Adjusted linear regression shows that with increases in N -formylmethionine abundance at ICU admission, 55 metabolites have significant differences common to both the VITdAL-ICU and RoCI cohorts. With increased N -formylmethionine abundance, both cohorts had elevations in individual short-chain acylcarnitine, branched chain amino acid, kynurenine pathway, and pentose phosphate pathway metabolites. Conclusions The results indicate that circulating N -formylmethionine promotes a metabolic shift with heightened mortality that involves incomplete mitochondrial fatty acid oxidation, increased branched chain amino acid metabolism, and activation of the pentose phosphate pathway. Graphic Abstract
AbstractList	Background Cell stress promotes degradation of mitochondria which release danger-associated molecular patterns that are catabolized to N -formylmethionine. We hypothesized that in critically ill adults, the response to N -formylmethionine is associated with increases in metabolomic shift-related metabolites and increases in 28-day mortality. Methods We performed metabolomics analyses on plasma from the 428-subject Correction of Vitamin D Deficiency in Critically Ill Patients trial (VITdAL-ICU) cohort and the 90-subject Brigham and Women’s Hospital Registry of Critical Illness (RoCI) cohort. In the VITdAL-ICU cohort, we analyzed 983 metabolites at Intensive Care Unit (ICU) admission, day 3, and 7. In the RoCI cohort, we analyzed 411 metabolites at ICU admission. The association between N -formylmethionine and mortality was determined by adjusted logistic regression. The relationship between individual metabolites and N -formylmethionine abundance was assessed with false discovery rate correction via linear regression, linear mixed-effects, and Gaussian graphical models. Results Patients with the top quartile of N -formylmethionine abundance at ICU admission had a significantly higher adjusted odds of 28-day mortality in the VITdAL-ICU (OR, 2.4; 95%CI 1.5–4.0; P = 0.001) and RoCI cohorts (OR, 5.1; 95%CI 1.4–18.7; P = 0.015). Adjusted linear regression shows that with increases in N -formylmethionine abundance at ICU admission, 55 metabolites have significant differences common to both the VITdAL-ICU and RoCI cohorts. With increased N -formylmethionine abundance, both cohorts had elevations in individual short-chain acylcarnitine, branched chain amino acid, kynurenine pathway, and pentose phosphate pathway metabolites. Conclusions The results indicate that circulating N -formylmethionine promotes a metabolic shift with heightened mortality that involves incomplete mitochondrial fatty acid oxidation, increased branched chain amino acid metabolism, and activation of the pentose phosphate pathway. Graphic Abstract Abstract Background Cell stress promotes degradation of mitochondria which release danger-associated molecular patterns that are catabolized to N-formylmethionine. We hypothesized that in critically ill adults, the response to N-formylmethionine is associated with increases in metabolomic shift-related metabolites and increases in 28-day mortality. Methods We performed metabolomics analyses on plasma from the 428-subject Correction of Vitamin D Deficiency in Critically Ill Patients trial (VITdAL-ICU) cohort and the 90-subject Brigham and Women’s Hospital Registry of Critical Illness (RoCI) cohort. In the VITdAL-ICU cohort, we analyzed 983 metabolites at Intensive Care Unit (ICU) admission, day 3, and 7. In the RoCI cohort, we analyzed 411 metabolites at ICU admission. The association between N-formylmethionine and mortality was determined by adjusted logistic regression. The relationship between individual metabolites and N-formylmethionine abundance was assessed with false discovery rate correction via linear regression, linear mixed-effects, and Gaussian graphical models. Results Patients with the top quartile of N-formylmethionine abundance at ICU admission had a significantly higher adjusted odds of 28-day mortality in the VITdAL-ICU (OR, 2.4; 95%CI 1.5–4.0; P = 0.001) and RoCI cohorts (OR, 5.1; 95%CI 1.4–18.7; P = 0.015). Adjusted linear regression shows that with increases in N-formylmethionine abundance at ICU admission, 55 metabolites have significant differences common to both the VITdAL-ICU and RoCI cohorts. With increased N-formylmethionine abundance, both cohorts had elevations in individual short-chain acylcarnitine, branched chain amino acid, kynurenine pathway, and pentose phosphate pathway metabolites. Conclusions The results indicate that circulating N-formylmethionine promotes a metabolic shift with heightened mortality that involves incomplete mitochondrial fatty acid oxidation, increased branched chain amino acid metabolism, and activation of the pentose phosphate pathway. Graphic Abstract Cell stress promotes degradation of mitochondria which release danger-associated molecular patterns that are catabolized to N-formylmethionine. We hypothesized that in critically ill adults, the response to N-formylmethionine is associated with increases in metabolomic shift-related metabolites and increases in 28-day mortality. We performed metabolomics analyses on plasma from the 428-subject Correction of Vitamin D Deficiency in Critically Ill Patients trial (VITdAL-ICU) cohort and the 90-subject Brigham and Women's Hospital Registry of Critical Illness (RoCI) cohort. In the VITdAL-ICU cohort, we analyzed 983 metabolites at Intensive Care Unit (ICU) admission, day 3, and 7. In the RoCI cohort, we analyzed 411 metabolites at ICU admission. The association between N-formylmethionine and mortality was determined by adjusted logistic regression. The relationship between individual metabolites and N-formylmethionine abundance was assessed with false discovery rate correction via linear regression, linear mixed-effects, and Gaussian graphical models. Patients with the top quartile of N-formylmethionine abundance at ICU admission had a significantly higher adjusted odds of 28-day mortality in the VITdAL-ICU (OR, 2.4; 95%CI 1.5-4.0; P = 0.001) and RoCI cohorts (OR, 5.1; 95%CI 1.4-18.7; P = 0.015). Adjusted linear regression shows that with increases in N-formylmethionine abundance at ICU admission, 55 metabolites have significant differences common to both the VITdAL-ICU and RoCI cohorts. With increased N-formylmethionine abundance, both cohorts had elevations in individual short-chain acylcarnitine, branched chain amino acid, kynurenine pathway, and pentose phosphate pathway metabolites. The results indicate that circulating N-formylmethionine promotes a metabolic shift with heightened mortality that involves incomplete mitochondrial fatty acid oxidation, increased branched chain amino acid metabolism, and activation of the pentose phosphate pathway. Background Cell stress promotes degradation of mitochondria which release danger-associated molecular patterns that are catabolized to N-formylmethionine. We hypothesized that in critically ill adults, the response to N-formylmethionine is associated with increases in metabolomic shift-related metabolites and increases in 28-day mortality. Methods We performed metabolomics analyses on plasma from the 428-subject Correction of Vitamin D Deficiency in Critically Ill Patients trial (VITdAL-ICU) cohort and the 90-subject Brigham and Women's Hospital Registry of Critical Illness (RoCI) cohort. In the VITdAL-ICU cohort, we analyzed 983 metabolites at Intensive Care Unit (ICU) admission, day 3, and 7. In the RoCI cohort, we analyzed 411 metabolites at ICU admission. The association between N-formylmethionine and mortality was determined by adjusted logistic regression. The relationship between individual metabolites and N-formylmethionine abundance was assessed with false discovery rate correction via linear regression, linear mixed-effects, and Gaussian graphical models. Results Patients with the top quartile of N-formylmethionine abundance at ICU admission had a significantly higher adjusted odds of 28-day mortality in the VITdAL-ICU (OR, 2.4; 95%CI 1.5-4.0; P = 0.001) and RoCI cohorts (OR, 5.1; 95%CI 1.4-18.7; P = 0.015). Adjusted linear regression shows that with increases in N-formylmethionine abundance at ICU admission, 55 metabolites have significant differences common to both the VITdAL-ICU and RoCI cohorts. With increased N-formylmethionine abundance, both cohorts had elevations in individual short-chain acylcarnitine, branched chain amino acid, kynurenine pathway, and pentose phosphate pathway metabolites. Conclusions The results indicate that circulating N-formylmethionine promotes a metabolic shift with heightened mortality that involves incomplete mitochondrial fatty acid oxidation, increased branched chain amino acid metabolism, and activation of the pentose phosphate pathway. Graphic Keywords: Metabolomics, N-formylmethionine, Critical illness, Acylcarnitine, Metabolic shift, Pentose phosphate pathway, Branched chain amino acids Cell stress promotes degradation of mitochondria which release danger-associated molecular patterns that are catabolized to N-formylmethionine. We hypothesized that in critically ill adults, the response to N-formylmethionine is associated with increases in metabolomic shift-related metabolites and increases in 28-day mortality.BACKGROUNDCell stress promotes degradation of mitochondria which release danger-associated molecular patterns that are catabolized to N-formylmethionine. We hypothesized that in critically ill adults, the response to N-formylmethionine is associated with increases in metabolomic shift-related metabolites and increases in 28-day mortality.We performed metabolomics analyses on plasma from the 428-subject Correction of Vitamin D Deficiency in Critically Ill Patients trial (VITdAL-ICU) cohort and the 90-subject Brigham and Women's Hospital Registry of Critical Illness (RoCI) cohort. In the VITdAL-ICU cohort, we analyzed 983 metabolites at Intensive Care Unit (ICU) admission, day 3, and 7. In the RoCI cohort, we analyzed 411 metabolites at ICU admission. The association between N-formylmethionine and mortality was determined by adjusted logistic regression. The relationship between individual metabolites and N-formylmethionine abundance was assessed with false discovery rate correction via linear regression, linear mixed-effects, and Gaussian graphical models.METHODSWe performed metabolomics analyses on plasma from the 428-subject Correction of Vitamin D Deficiency in Critically Ill Patients trial (VITdAL-ICU) cohort and the 90-subject Brigham and Women's Hospital Registry of Critical Illness (RoCI) cohort. In the VITdAL-ICU cohort, we analyzed 983 metabolites at Intensive Care Unit (ICU) admission, day 3, and 7. In the RoCI cohort, we analyzed 411 metabolites at ICU admission. The association between N-formylmethionine and mortality was determined by adjusted logistic regression. The relationship between individual metabolites and N-formylmethionine abundance was assessed with false discovery rate correction via linear regression, linear mixed-effects, and Gaussian graphical models.Patients with the top quartile of N-formylmethionine abundance at ICU admission had a significantly higher adjusted odds of 28-day mortality in the VITdAL-ICU (OR, 2.4; 95%CI 1.5-4.0; P = 0.001) and RoCI cohorts (OR, 5.1; 95%CI 1.4-18.7; P = 0.015). Adjusted linear regression shows that with increases in N-formylmethionine abundance at ICU admission, 55 metabolites have significant differences common to both the VITdAL-ICU and RoCI cohorts. With increased N-formylmethionine abundance, both cohorts had elevations in individual short-chain acylcarnitine, branched chain amino acid, kynurenine pathway, and pentose phosphate pathway metabolites.RESULTSPatients with the top quartile of N-formylmethionine abundance at ICU admission had a significantly higher adjusted odds of 28-day mortality in the VITdAL-ICU (OR, 2.4; 95%CI 1.5-4.0; P = 0.001) and RoCI cohorts (OR, 5.1; 95%CI 1.4-18.7; P = 0.015). Adjusted linear regression shows that with increases in N-formylmethionine abundance at ICU admission, 55 metabolites have significant differences common to both the VITdAL-ICU and RoCI cohorts. With increased N-formylmethionine abundance, both cohorts had elevations in individual short-chain acylcarnitine, branched chain amino acid, kynurenine pathway, and pentose phosphate pathway metabolites.The results indicate that circulating N-formylmethionine promotes a metabolic shift with heightened mortality that involves incomplete mitochondrial fatty acid oxidation, increased branched chain amino acid metabolism, and activation of the pentose phosphate pathway.CONCLUSIONSThe results indicate that circulating N-formylmethionine promotes a metabolic shift with heightened mortality that involves incomplete mitochondrial fatty acid oxidation, increased branched chain amino acid metabolism, and activation of the pentose phosphate pathway. Cell stress promotes degradation of mitochondria which release danger-associated molecular patterns that are catabolized to N-formylmethionine. We hypothesized that in critically ill adults, the response to N-formylmethionine is associated with increases in metabolomic shift-related metabolites and increases in 28-day mortality. We performed metabolomics analyses on plasma from the 428-subject Correction of Vitamin D Deficiency in Critically Ill Patients trial (VITdAL-ICU) cohort and the 90-subject Brigham and Women's Hospital Registry of Critical Illness (RoCI) cohort. In the VITdAL-ICU cohort, we analyzed 983 metabolites at Intensive Care Unit (ICU) admission, day 3, and 7. In the RoCI cohort, we analyzed 411 metabolites at ICU admission. The association between N-formylmethionine and mortality was determined by adjusted logistic regression. The relationship between individual metabolites and N-formylmethionine abundance was assessed with false discovery rate correction via linear regression, linear mixed-effects, and Gaussian graphical models. The results indicate that circulating N-formylmethionine promotes a metabolic shift with heightened mortality that involves incomplete mitochondrial fatty acid oxidation, increased branched chain amino acid metabolism, and activation of the pentose phosphate pathway.
ArticleNumber	321
Audience	Academic
Author	Karin Amrein Mayra Pinilla-Vera Jessica A. Lasky-Su Rebecca M. Baron Martin Ingi Sigurdsson Hirotada Kobayashi Laura E. Fredenburgh Kenneth B. Christopher Kiichi Nakahira Angela J. Rogers
Author_xml	– sequence: 1 givenname: Martin Ingi surname: Sigurdsson fullname: Sigurdsson, Martin Ingi organization: Anesthesiology and Critical Care Medicine, Landspitali University Hospital, University of Iceland, Faculty of Medicine, University of Iceland – sequence: 2 givenname: Hirotada surname: Kobayashi fullname: Kobayashi, Hirotada organization: Division of Renal Medicine, Brigham and Women’s Hospital – sequence: 3 givenname: Karin surname: Amrein fullname: Amrein, Karin organization: Division of Endocrinology and Diabetology, Medical University of Graz – sequence: 4 givenname: Kiichi surname: Nakahira fullname: Nakahira, Kiichi organization: Nara Medical University, Weill Cornell Medicine – sequence: 5 givenname: Angela J. surname: Rogers fullname: Rogers, Angela J. organization: Stanford University Medical Center – sequence: 6 givenname: Mayra surname: Pinilla-Vera fullname: Pinilla-Vera, Mayra organization: Division of Pulmonary and Critical Care Medicine, Brigham and Women’s Hospital – sequence: 7 givenname: Rebecca M. surname: Baron fullname: Baron, Rebecca M. organization: Division of Pulmonary and Critical Care Medicine, Brigham and Women’s Hospital – sequence: 8 givenname: Laura E. surname: Fredenburgh fullname: Fredenburgh, Laura E. organization: Division of Pulmonary and Critical Care Medicine, Brigham and Women’s Hospital – sequence: 9 givenname: Jessica A. surname: Lasky-Su fullname: Lasky-Su, Jessica A. organization: Channing Division of Network Medicine, Brigham and Women’s Hospital – sequence: 10 givenname: Kenneth B. surname: Christopher fullname: Christopher, Kenneth B. email: kbchristopher@bwh.harvard.edu organization: Division of Renal Medicine, Brigham and Women’s Hospital, Channing Division of Network Medicine, Brigham and Women’s Hospital
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Cites_doi	10.1371/journal.pone.0087538 10.1016/S0026-0495(99)90179-8 10.1016/j.xcrm.2022.100652 10.1146/annurev-physiol-020518-114455 10.1007/s11306-007-0099-6 10.1186/s40635-016-0094-1 10.1002/cem.1187 10.1089/ars.2015.6407 10.1038/s41586-021-03767-x 10.1186/s13054-018-2275-7 10.1371/journal.pmed.1001577 10.1038/s41598-022-10415-5 10.1016/j.chest.2019.09.028 10.1111/j.2517-6161.1995.tb02031.x 10.1016/j.coisb.2017.04.003 10.1371/journal.pgen.1002215 10.1089/ars.2010.3797 10.1038/nrm.2016.25 10.1016/j.cmet.2007.10.013 10.1186/s13054-019-2670-8 10.1016/j.bbamcr.2018.11.015 10.1093/bja/aeu187 10.1186/1752-0509-5-21 10.1164/rccm.201201-0003OC 10.1038/35047123 10.3390/metabo9070128 10.1096/fasebj.8.2.8119488 10.1016/j.ebiom.2022.103918 10.1038/nri2873 10.1021/acs.jproteome.7b00160 10.2174/2213235X04666160613122429 10.1038/s41540-017-0029-9 10.1016/j.cmet.2012.01.024 10.1084/jem.180.6.2191 10.1016/j.clnu.2020.09.028 10.1097/CCM.0000000000001740 10.1007/978-1-0716-0239-3_17 10.1016/S0022-2836(63)80096-0 10.1002/cem.785 10.1016/S2213-2600(14)70290-5 10.1038/nrm3314 10.1016/j.jaut.2021.102630 10.1016/j.bjae.2019.03.002 10.1161/CIRCGENETICS.113.000123 10.3389/fimmu.2015.00422 10.1164/rccm.201003-0326OC 10.1007/s00134-013-2935-7 10.1038/s41598-021-83602-5 10.1097/SHK.0b013e318167378f 10.1136/thoraxjnl-2017-211073 10.1001/jama.2014.13204
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Keywords	Metabolic shift Metabolomics Critical illness Branched chain amino acids formylmethionine Acylcarnitine Pentose phosphate pathway N-formylmethionine
Language	English
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PublicationYear	2022
Publisher	Springer Science and Business Media LLC BioMed Central BioMed Central Ltd BMC
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References	M Nalos (4174_CR48) 2016; 4 GY Chen (4174_CR9) 2010; 10 PG Haji-Michael (4174_CR47) 1999; 48 CB Newgard (4174_CR44) 2012; 15 B Duvvuri (4174_CR52) 2021; 119 C-H Initiative (4174_CR4) 2021; 600 JA Westerhuis (4174_CR28) 2008; 4 4174_CR35 JL Gao (4174_CR39) 1994; 180 A Kruger (4174_CR46) 2011; 15 BP Scicluna (4174_CR1) 2022; 77 AJ Rogers (4174_CR18) 2014; 9 L Eriksson (4174_CR29) 2008; 22 ZA Puthucheary (4174_CR32) 2018; 73 N Desai (4174_CR53) 2019; 19 JC Preiser (4174_CR31) 2014; 113 D Braga (4174_CR2) 2019; 23 B Matthew (4174_CR21) 2003; 17 E Venereau (4174_CR33) 2015; 6 JE Carre (4174_CR6) 2010; 182 K Amrein (4174_CR3) 2021; 40 CH Johnson (4174_CR14) 2016; 17 A Frishberg (4174_CR5) 2022; 2022 M Neinast (4174_CR43) 2019; 81 K Nakahira (4174_CR30) 2013; 10 RF Kletzien (4174_CR45) 1994; 8 GJ Patti (4174_CR50) 2012; 13 M Garcia-Contreras (4174_CR38) 2017; 16 S Chary (4174_CR16) 2021; 11 CA Raabe (4174_CR13) 2019; 1866 J Krumsiek (4174_CR26) 2011; 5 CW Seymour (4174_CR41) 2013; 39 LR Thistlethwaite (4174_CR49) 2022; 12 K Mittelstrass (4174_CR34) 2011; 7 K Amrein (4174_CR15) 2014; 312 S Neugebauer (4174_CR51) 2016; 44 B Worley (4174_CR22) 2016; 4 JP Waller (4174_CR37) 1963; 7 T Dolinay (4174_CR17) 2012; 185 PI Johansson (4174_CR11) 2018; 22 HE Faust (4174_CR12) 2020; 157 TR Koves (4174_CR42) 2008; 7 J Chong (4174_CR19) 2020; 2104 M Henglin (4174_CR24) 2019; 9 A Rautanen (4174_CR7) 2015; 3 KT Do (4174_CR27) 2017; 3 K Nakahira (4174_CR10) 2015; 23 B Levy (4174_CR40) 2008; 30 Y Benjamini (4174_CR20) 1995; 57 4174_CR23 CD Russell (4174_CR8) 2017; 2 H Hemmi (4174_CR36) 2000; 408 B Zhang (4174_CR25) 2014; 7
References_xml	– volume: 9 start-page: e87538 issue: 1 year: 2014 ident: 4174_CR18 publication-title: PLoS ONE doi: 10.1371/journal.pone.0087538 – volume: 48 start-page: 779 issue: 6 year: 1999 ident: 4174_CR47 publication-title: Metabolism doi: 10.1016/S0026-0495(99)90179-8 – volume: 2022 start-page: 100652 year: 2022 ident: 4174_CR5 publication-title: Cell Rep Med doi: 10.1016/j.xcrm.2022.100652 – volume: 81 start-page: 139 year: 2019 ident: 4174_CR43 publication-title: Annu Rev Physiol doi: 10.1146/annurev-physiol-020518-114455 – volume: 4 start-page: 81 issue: 1 year: 2008 ident: 4174_CR28 publication-title: Metabolomics doi: 10.1007/s11306-007-0099-6 – volume: 4 start-page: 21 issue: 1 year: 2016 ident: 4174_CR48 publication-title: Intensive Care Med Exp doi: 10.1186/s40635-016-0094-1 – volume: 22 start-page: 594 issue: 11–12 year: 2008 ident: 4174_CR29 publication-title: J Chemom doi: 10.1002/cem.1187 – volume: 23 start-page: 1329 issue: 17 year: 2015 ident: 4174_CR10 publication-title: Antioxid Redox Signal doi: 10.1089/ars.2015.6407 – volume: 600 start-page: 472 issue: 7889 year: 2021 ident: 4174_CR4 publication-title: Nature doi: 10.1038/s41586-021-03767-x – volume: 22 start-page: 360 issue: 1 year: 2018 ident: 4174_CR11 publication-title: Crit Care doi: 10.1186/s13054-018-2275-7 – volume: 10 start-page: e1001577 issue: 12 year: 2013 ident: 4174_CR30 publication-title: PLoS Med doi: 10.1371/journal.pmed.1001577 – volume: 12 start-page: 6556 issue: 1 year: 2022 ident: 4174_CR49 publication-title: Sci Rep doi: 10.1038/s41598-022-10415-5 – volume: 157 start-page: 67 issue: 1 year: 2020 ident: 4174_CR12 publication-title: Chest doi: 10.1016/j.chest.2019.09.028 – volume: 57 start-page: 289 year: 1995 ident: 4174_CR20 publication-title: J R Stat Soc Ser B (Methodol) doi: 10.1111/j.2517-6161.1995.tb02031.x – volume: 2 start-page: 140 year: 2017 ident: 4174_CR8 publication-title: Curr Opin Syst Biol doi: 10.1016/j.coisb.2017.04.003 – volume: 7 start-page: e1002215 issue: 8 year: 2011 ident: 4174_CR34 publication-title: PLoS Genet doi: 10.1371/journal.pgen.1002215 – volume: 15 start-page: 311 issue: 2 year: 2011 ident: 4174_CR46 publication-title: Antioxid Redox Signal doi: 10.1089/ars.2010.3797 – volume: 17 start-page: 451 issue: 7 year: 2016 ident: 4174_CR14 publication-title: Nat Rev Mol Cell Biol doi: 10.1038/nrm.2016.25 – volume: 7 start-page: 45 issue: 1 year: 2008 ident: 4174_CR42 publication-title: Cell Metab doi: 10.1016/j.cmet.2007.10.013 – volume: 23 start-page: 414 issue: 1 year: 2019 ident: 4174_CR2 publication-title: Crit Care doi: 10.1186/s13054-019-2670-8 – ident: 4174_CR35 – volume: 1866 start-page: 305 issue: 2 year: 2019 ident: 4174_CR13 publication-title: Biochim Biophys Acta Mol Cell Res doi: 10.1016/j.bbamcr.2018.11.015 – volume: 113 start-page: 945 issue: 6 year: 2014 ident: 4174_CR31 publication-title: Br J Anaesth doi: 10.1093/bja/aeu187 – volume: 5 start-page: 21 year: 2011 ident: 4174_CR26 publication-title: BMC Syst Biol doi: 10.1186/1752-0509-5-21 – volume: 185 start-page: 1225 issue: 11 year: 2012 ident: 4174_CR17 publication-title: Am J Respir Crit Care Med doi: 10.1164/rccm.201201-0003OC – volume: 408 start-page: 740 issue: 6813 year: 2000 ident: 4174_CR36 publication-title: Nature doi: 10.1038/35047123 – volume: 9 start-page: 128 issue: 7 year: 2019 ident: 4174_CR24 publication-title: Metabolites doi: 10.3390/metabo9070128 – ident: 4174_CR23 – volume: 8 start-page: 174 issue: 2 year: 1994 ident: 4174_CR45 publication-title: FASEB J doi: 10.1096/fasebj.8.2.8119488 – volume: 77 start-page: 103918 year: 2022 ident: 4174_CR1 publication-title: EBioMedicine doi: 10.1016/j.ebiom.2022.103918 – volume: 10 start-page: 826 issue: 12 year: 2010 ident: 4174_CR9 publication-title: Nat Rev Immunol doi: 10.1038/nri2873 – volume: 16 start-page: 2294 issue: 6 year: 2017 ident: 4174_CR38 publication-title: J Proteome Res doi: 10.1021/acs.jproteome.7b00160 – volume: 4 start-page: 97 issue: 2 year: 2016 ident: 4174_CR22 publication-title: Curr Metab doi: 10.2174/2213235X04666160613122429 – volume: 3 start-page: 28 year: 2017 ident: 4174_CR27 publication-title: NPJ Syst Biol Appl doi: 10.1038/s41540-017-0029-9 – volume: 15 start-page: 606 issue: 5 year: 2012 ident: 4174_CR44 publication-title: Cell Metab doi: 10.1016/j.cmet.2012.01.024 – volume: 180 start-page: 2191 issue: 6 year: 1994 ident: 4174_CR39 publication-title: J Exp Med doi: 10.1084/jem.180.6.2191 – volume: 40 start-page: 2053 issue: 4 year: 2021 ident: 4174_CR3 publication-title: Clin Nutr doi: 10.1016/j.clnu.2020.09.028 – volume: 44 start-page: 1649 issue: 9 year: 2016 ident: 4174_CR51 publication-title: Crit Care Med doi: 10.1097/CCM.0000000000001740 – volume: 2104 start-page: 337 year: 2020 ident: 4174_CR19 publication-title: Methods Mol Biol doi: 10.1007/978-1-0716-0239-3_17 – volume: 7 start-page: 483 year: 1963 ident: 4174_CR37 publication-title: J Mol Biol doi: 10.1016/S0022-2836(63)80096-0 – volume: 17 start-page: 166 issue: 3 year: 2003 ident: 4174_CR21 publication-title: J Chemom doi: 10.1002/cem.785 – volume: 3 start-page: 53 issue: 1 year: 2015 ident: 4174_CR7 publication-title: Lancet Respir Med doi: 10.1016/S2213-2600(14)70290-5 – volume: 13 start-page: 263 issue: 4 year: 2012 ident: 4174_CR50 publication-title: Nat Rev Mol Cell Biol doi: 10.1038/nrm3314 – volume: 119 start-page: 102630 year: 2021 ident: 4174_CR52 publication-title: J Autoimmun doi: 10.1016/j.jaut.2021.102630 – volume: 19 start-page: 212 issue: 7 year: 2019 ident: 4174_CR53 publication-title: BJA Educ doi: 10.1016/j.bjae.2019.03.002 – volume: 7 start-page: 536 issue: 4 year: 2014 ident: 4174_CR25 publication-title: Circ Cardiovasc Genet doi: 10.1161/CIRCGENETICS.113.000123 – volume: 6 start-page: 422 year: 2015 ident: 4174_CR33 publication-title: Front Immunol doi: 10.3389/fimmu.2015.00422 – volume: 182 start-page: 745 issue: 6 year: 2010 ident: 4174_CR6 publication-title: Am J Respir Crit Care Med doi: 10.1164/rccm.201003-0326OC – volume: 39 start-page: 1423 issue: 8 year: 2013 ident: 4174_CR41 publication-title: Intensive Care Med doi: 10.1007/s00134-013-2935-7 – volume: 11 start-page: 3951 year: 2021 ident: 4174_CR16 publication-title: Sci Rep doi: 10.1038/s41598-021-83602-5 – volume: 30 start-page: 417 issue: 4 year: 2008 ident: 4174_CR40 publication-title: Shock doi: 10.1097/SHK.0b013e318167378f – volume: 73 start-page: 926 issue: 10 year: 2018 ident: 4174_CR32 publication-title: Thorax doi: 10.1136/thoraxjnl-2017-211073 – volume: 312 start-page: 1520 issue: 15 year: 2014 ident: 4174_CR15 publication-title: JAMA doi: 10.1001/jama.2014.13204
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Snippet	Background Cell stress promotes degradation of mitochondria which release danger-associated molecular patterns that are catabolized to N -formylmethionine. We... Cell stress promotes degradation of mitochondria which release danger-associated molecular patterns that are catabolized to N-formylmethionine. We hypothesized... Background Cell stress promotes degradation of mitochondria which release danger-associated molecular patterns that are catabolized to N-formylmethionine. We... Abstract Background Cell stress promotes degradation of mitochondria which release danger-associated molecular patterns that are catabolized to...
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SubjectTerms	Acylcarnitine Adult Amino Acids, Branched-Chain Care and treatment Clinical Trials as Topic Critical Care Medicine Critical Illness Critically ill Emergency Medicine Fatty Acids Female Health aspects Hospital Mortality Humans Intensive Intensive Care Units Kynurenine Medical emergencies. Critical care. Intensive care. First aid Medicine Medicine & Public Health Metabolic shift Metabolomics Metabolomics - methods Methionine N-Formylmethionine Pentose phosphate pathway Prognosis RC86-88.9
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Title	Circulating N-formylmethionine and metabolic shift in critical illness: a multicohort metabolomics study
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