Evidence map›Paper›PMID 32068115›Full record

ReviewBiochimica et biophysica acta. Molecular basis of disease2020

Regulation of metabolism by mitochondrial enzyme acetylation in cardiac ischemia-reperfusion injury.

Daniel J Herr, Toolika Singh, Tajinder Dhammu, Donald R Menick

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta. Molecular basis of disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. The sirtuin family in health and disease.Signal transduction and targeted therapy · 2022
    Review
  9. Article
  10. Review
  11. Processed lateral root ofFrontiers in pharmacology · 2022
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Daniel J HerrDepartment of Medicine, Division of Cardiology, Medical University of South Carolina, Charleston, SC, United States of America.
Toolika SinghDepartment of Medicine, Division of Cardiology, Medical University of South Carolina, Charleston, SC, United States of America.
Tajinder DhammuDepartment of Medicine, Division of Cardiology, Medical University of South Carolina, Charleston, SC, United States of America.
Donald R MenickDepartment of Medicine, Division of Cardiology, Medical University of South Carolina, Charleston, SC, United States of America; Ralph H. Johnson Veterans Affairs Medical Center, Charleston, SC, United States of America. Electronic address: menickd@musc.edu.

Funding

TRAINING TO IMPROVE CARDIOVASCULAR THERAPIEST32HL007260 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI MENICK, DONALD R. · 1985 to 2021
$11.1M
South Carolina Clinical & Translational Research Institute (SCTR)UL1TR000062 · NCATS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADY, KATHLEEN T. · 2012 to 2014
$9.4M
TRAINING PROGRAM FOR MEDICAL SCIENTISTST32GM008716 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI DEMORE, NANCY · 1999 to 2024
$9.3M
South Carolina Clinical & Translational Research Institute (SCTR)TL1TR000061 · NCATS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADY, KATHLEEN T. · 2012 to 2014
$483k
Elucidating the role of class I HDACs in cardiac ischemia reperfusion injuryF30HL129629 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI HERR, DANIEL J · 2016 to 2018
$111k
Regulatroy Role of HDAC in Post-MI Ventricular RemodelingI01BX002327 · VA · RALPH H JOHNSON VA MEDICAL CENTER · PI MENICK, DONALD R. · 2015 to 2023
–
BLRD VA I01 BX002327NCATS NIH HHS TL1 TR000061NCATS NIH HHS UL1 TR000062NHLBI NIH HHS F30 HL129629NHLBI NIH HHS T32 HL007260NIGMS NIH HHS T32 GM008716
6 · The paper itself

Abstract

Ischemia reperfusion injury (I/R injury) contributes significantly to morbidity and mortality following myocardial infarction (MI). Although rapid reperfusion of the ischemic myocardium was established decades ago as a highly beneficial therapy for MI, significant cell death still occurs after the onset of reperfusion. Mitochondrial dysfunction is closely associated with I/R injury, resulting in the uncontrolled production of reactive oxygen species (ROS). Considerable efforts have gone into understanding the metabolic perturbations elicited by I/R injury. Recent work has identified the critical role of reversible protein acetylation in maintaining normal mitochondrial biologic function and energy metabolism both in the normal heart and during I/R injury. Several studies have shown that modification of class I HDAC and/or Sirtuin (Sirt) activity is cardioprotective in the setting of I/R injury. A better understanding of the role of these metabolic pathways in reperfusion injury and their regulation by reversible protein acetylation presents a promising way forward in improving the treatment of cardiac reperfusion injury. Here we briefly review some of what is known about how acetylation regulates mitochondrial metabolism and how it relates to I/R injury.

Indexed as

Energy MetabolismAcetylationAnimalsHumansMiceMitochondria, HeartMyocardial InfarctionMyocardial Reperfusion InjuryMyocardiumMyocytes, CardiacReactive Oxygen SpeciesReperfusion InjuryReactive Oxygen SpeciesHDAC inhibitorsHistone deacetylaseIschemia reperfusion injuryLysine acylationMitochondrial metabolism

Identifiers

PMID32068115
PMCPMC7872201

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.