Evidence map›Paper›PMID 34211627›Full record

ReviewOxidative medicine and cellular longevity2021

The Role of Mitochondrial Quality Control in Cardiac Ischemia/Reperfusion Injury.

Jia Huang, Ruibing Li, Chengbin Wang

Abstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed.

  1. Review
  2. Article
  3. Improvement of Cardiac Function by Polyclonal Antibodies Against CaInternational journal of molecular sciences · 2026
    Article
  4. Mitochondria as a Therapeutic Target in Metabolic Disorders.Mini reviews in medicinal chemistry · 2026
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Unbalanced Redox With Autophagy in Cardiovascular Disease.Journal of lipid and atherosclerosis · 2023
    Review
  17. Article
  18. Mechanistic study of optic atrophy 1 in ischemia-reperfusion disease.Journal of molecular medicine (Berlin, Germany) · 2023
    Review
  19. NLRP3-mediated inflammation in cardio-oncology: sterile yet harmful.Translational research : the journal of laboratory and clinical medicine · 2023
    Review
  20. 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

3 authors.

Jia HuangDepartment of Clinical Laboratory Medicine, the First Medical Centre, Chinese PLA General Hospital, China.
Ruibing LiDepartment of Clinical Laboratory Medicine, the First Medical Centre, Chinese PLA General Hospital, China.
Chengbin WangDepartment of Clinical Laboratory Medicine, the First Medical Centre, Chinese PLA General Hospital, China.ORCID https://orcid.org/0000-0002-6535-5967

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A healthy mitochondrial network produces a large amount of ATP and biosynthetic intermediates to provide sufficient energy for myocardium and maintain normal cell metabolism. Mitochondria form a dynamic and interconnected network involved in various cellular metabolic signaling pathways. As mitochondria are damaged, controlling mitochondrial quantity and quality is activated by changing their morphology and tube network structure, mitophagy, and biogenesis to replenish a healthy mitochondrial network to preserve cell function. There is no doubt that mitochondrial dysfunction has become a key factor in many diseases. Ischemia/reperfusion (IR) injury is a pathological manifestation of various heart diseases. Cardiac ischemia causes temporary tissue and organelle damage. Although reperfusion is essential to compensate for nutrient deficiency, blood flow restoration inconsequently further kills the previously ischemic cardiomyocytes. To date, dysfunctional mitochondria and disturbed mitochondrial quality control have been identified as critical IR injury mechanisms. Many researchers have detected abnormal mitochondrial morphology and mitophagy, as well as aberrant levels and activity of mitochondrial biogenesis factors in the IR injury model. Although mitochondrial damage is well-known in myocardial IR injury, the causal relationship between abnormal mitochondrial quality control and IR injury has not been established. This review briefly describes the molecular mechanisms of mitochondrial quality control, summarizes our current understanding of the complex role of mitochondrial quality control in IR injury, and finally speculates on the possibility of targeted control of mitochondria and the methods available to mitigate IR injury.

Indexed as

HumansMitochondria, HeartMyocardial IschemiaMyocytes, CardiacReperfusion Injury

Identifiers

PMID34211627
PMCPMC8211512

What OpenQuestion holds

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LicenceCC BY
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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.