Evidence map›Paper›PMID 27860548›Full record

ReviewAnnual review of pharmacology and toxicology2017

Mitochondrial Dysfunction and Myocardial Ischemia-Reperfusion: Implications for Novel Therapies.

Edward J Lesnefsky, Qun Chen, Bernard Tandler, Charles L Hoppel

Open access · greenAbstract readReview
In one paragraph

Review in Annual review of pharmacology and toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 237 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
237citing papers in PubMed, 1 pooled it
17.9field-weighted citation impact, top 1% of its field
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

237 citing papers in PubMed, 1 synthesis or guideline pooled it, 417 citations in OpenAlex.

  1. Pooled it
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  4. Timed metabolic repair after myocardial infarction.Nature cardiovascular research · 2026
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177 more citing papers are in PubMed but not listed here.

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 at 3 institutions in 1 country.

Edward J LesnefskyDepartment of Medicine, Division of Cardiology, Pauley Heart Center, Virginia Commonwealth University, Richmond, Virginia 23298; email: edward.lesnefsky@vcuhealth.org , qun.chen@vcuhealth.org.
Qun ChenDepartment of Medicine, Division of Cardiology, Pauley Heart Center, Virginia Commonwealth University, Richmond, Virginia 23298; email: edward.lesnefsky@vcuhealth.org , qun.chen@vcuhealth.org.
Bernard TandlerDepartment of Biological Sciences, Case Western Reserve University School of Dental Medicine, Cleveland, Ohio 44106; email: bernard.tandler@case.edu.
Charles L HoppelDepartment of Pharmacology, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106; email: charles.hoppel@case.edu.
Virginia Commonwealth University · USCase Western Reserve University · USUniversity School · US

Funding

Center for Clinical and Translational ResearchUL1TR000058 · NCATS · VIRGINIA COMMONWEALTH UNIVERSITY · PI MOELLER, FREDERICK GERARD · 2012 to 2015
$12.5M
Aged rat heart mitochondrial dysfunction: proteome and lipidome dynamicsR21AG049461 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI HOPPEL, CHARLES LESLIE · 2015 to 2015
$238k
Reduction of cardiac injury by targeting damaged mitochondria during reperfusionI01BX001355 · VA · VA VETERANS ADMINISTRATION HOSPITAL · PI LESNEFSKY, EDWARD J · 2012 to 2025
–
American Heart Association-American Stroke Association 15GRNT24480123BLRD VA I01 BX001355NCATS NIH HHS UL1 TR000058NIA NIH HHS R21 AG049461
6 · The paper itself

Abstract

Mitochondria have emerged as key participants in and regulators of myocardial injury during ischemia and reperfusion. This review examines the sites of damage to cardiac mitochondria during ischemia and focuses on the impact of these defects. The concept that mitochondrial damage during ischemia leads to cardiac injury during reperfusion is addressed. The mechanisms that translate ischemic mitochondrial injury into cellular damage, during both ischemia and early reperfusion, are examined. Next, we discuss strategies that modulate and counteract these mechanisms of mitochondrial-driven injury. The new concept that mitochondria are not merely stochastic sites of oxidative and calcium-mediated injury but that they activate cellular responses of mitochondrial remodeling and cellular reactions that modulate the balance between cell death and recovery is reviewed, and the therapeutic implications of this concept are discussed.

Indexed as

AnimalsCardiovascular AgentsCell DeathElectron TransportHumansIschemic Preconditioning, MyocardialMitochondria, HeartMyocardial Reperfusion InjuryCardiovascular Agentscardiolipinelectron transport chainfatty acid oxidationoxidative phosphorylationreactive oxygen speciesubiquinol:cytochrome c oxidoreductase

Identifiers

PMID27860548
PMCPMC11060135
OpenAlexW2555339002

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.