Evidence map›Paper›PMID 31590423›Full record

ReviewAntioxidants (Basel, Switzerland)2019

The Role of Mitochondria in the Mechanisms of Cardiac Ischemia-Reperfusion Injury.

Andrey V Kuznetsov, Sabzali Javadov, Raimund Margreiter, Michael Grimm, Judith Hagenbuchner, Michael J Ausserlechner

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed, 4 pooled it
8.1field-weighted citation impact, top 2% 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

120 citing papers in PubMed, 4 syntheses or guidelines pooled it, 192 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. A perspective on the future of heart failure research.Journal of molecular and cellular cardiology plus · 2026
    Article
  13. Review
  14. Review
  15. Review
  16. Mitochondrial Adaptation to Mechanical Stress in Cardiac Ageing and Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  17. Review
  18. Article
  19. Article
  20. Article

60 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

6 authors at 2 institutions in 2 countries.

Andrey V KuznetsovCardiac Surgery Research Laboratory, Department of Cardiac Surgery, Medical University of Innsbruck, Innsbruck A-6020, Austria. andrey.kuznetsov@tirol-kliniken.at.
Sabzali JavadovDepartment of Physiology, School of Medicine, University of Puerto Rico, San Juan, PR 00936-5067, USA.
Raimund MargreiterDepartment of Visceral, Transplant and Thoracic Surgery, Medical University of Innsbruck, Innsbruck A-6020, Austria.
Michael GrimmCardiac Surgery Research Laboratory, Department of Cardiac Surgery, Medical University of Innsbruck, Innsbruck A-6020, Austria.
Judith HagenbuchnerDepartment of Pediatrics II, Medical University of Innsbruck, Innsbruck A-6020, Austria.
Michael J AusserlechnerDepartment of Pediatrics I, Medical University of Innsbruck, Innsbruck A-6020, Austria. michael.j.ausserlechner@i-med.ac.at.
Innsbruck Medical University · ATUniversity of Puerto Rico System · PR

Funding

Crosstalk between mitochondrial permeability transition and ETC supercomplexes in myocardial infarctionSC1GM128210 · NIGMS · UNIVERSITY OF PUERTO RICO MED SCIENCES · PI JAVADOV, SABZALI · 2017 to 2019
$1.1M
Austrian Science Fund Project I3089-B28Austrian Science Fund FWF I 3089NIGMS NIH HHS SC1 GM128210NIH HHS NIH Grant SC1GM128210
6 · The paper itself

Abstract

Mitochondria play a critical role in maintaining cellular function by ATP production. They are also a source of reactive oxygen species (ROS) and proapoptotic factors. The role of mitochondria has been established in many aspects of cell physiology/pathophysiology, including cell signaling. Mitochondria may deteriorate under various pathological conditions, including ischemia-reperfusion (IR) injury. Mitochondrial injury can be one of the main causes for cardiac and other tissue injuries by energy stress and overproduction of toxic reactive oxygen species, leading to oxidative stress, elevated calcium and apoptotic and necrotic cell death. However, the interplay among these processes in normal and pathological conditions is still poorly understood. Mitochondria play a critical role in cardiac IR injury, where they are directly involved in several pathophysiological mechanisms. We also discuss the role of mitochondria in the context of mitochondrial dynamics, specializations and heterogeneity. Also, we wanted to stress the existence of morphologically and functionally different mitochondrial subpopulations in the heart that may have different sensitivities to diseases and IR injury. Therefore, various cardioprotective interventions that modulate mitochondrial stability, dynamics and turnover, including various pharmacologic agents, specific mitochondrial antioxidants and uncouplers, and ischemic preconditioning can be considered as the main strategies to protect mitochondrial and cardiovascular function and thus enhance longevity.

Indexed as

cytoskeletonenergy metabolismheartischemia-reperfusionmitochondriamitochondrial heterogeneitypreconditioningreactive oxygen speciessignaling

Identifiers

PMID31590423
PMCPMC6826663
OpenAlexW2979032726

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.