Evidence map›Paper›PMID 34965154›Full record

ReviewAmerican journal of physiology. Cell physiology2022

Mitochondrial quality surveillance: mitophagy in cardiovascular health and disease.

Rachel Y Diao, Åsa B Gustafsson

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Cell physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Mitochondrial Dysfunction in Congenital Heart Disease.Journal of cardiovascular development and disease · 2025
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Hallmarks of cardiovascular ageing.Nature reviews. Cardiology · 2023
    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

2 authors at 1 institution in 1 country.

Rachel Y DiaoSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, California.
Åsa B GustafssonSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, California.ORCID 0000-0001-6347-8210
University of California San Diego · US

Funding

GRADUATE TRAINING IN CELLULAR &MOLECULAR PHARMACOLOGYT32GM007752 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROWN, JOAN HELLER, HANDEL, TRACY M · 1985 to 2023
$13.5M
Secretion of mitochondria as a cellular quality control mechanismR01HL155281 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUSTAFSSON, ASA B. · 2021 to 2024
$2.3M
Autophagy and Megamitochondria in Cardiac Aging and Heart FailureR01HL157265 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUSTAFSSON, ASA B. · 2021 to 2024
$1.9M
MCL-1 is a critical regulator of mitochondrial dynamics and function in myocytesR01HL132300 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUSTAFSSON, ASA B. · 2017 to 2020
$1.7M
Role of the Endosomal-Lysosomal Pathway in Mitochondrial Quality ControlR01HL138560 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUSTAFSSON, ASA B. · 2017 to 2020
$1.6M
HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL157265HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01HL132300HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01HL138560HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01HL155281HHS | NIH | National Institute of General Medical Sciences (NIGMS) T32GM007752NHLBI NIH HHS R01 HL132300NHLBI NIH HHS R01 HL138560NHLBI NIH HHS R01 HL155281NHLBI NIH HHS R01 HL157265NIGMS NIH HHS T32 GM007752
6 · The paper itself

Abstract

Selective autophagy of mitochondria, known as mitophagy, is a major quality control pathway in the heart that is involved in removing unwanted or dysfunctional mitochondria from the cell. Baseline mitophagy is critical for maintaining fitness of the mitochondrial network by continuous turnover of aged and less-functional mitochondria. Mitophagy is also critical in adapting to stress associated with mitochondrial damage or dysfunction. The removal of damaged mitochondria prevents reactive oxygen species-mediated damage to proteins and DNA and suppresses activation of inflammation and cell death. Impairments in mitophagy are associated with the pathogenesis of many diseases, including cancers, inflammatory diseases, neurodegeneration, and cardiovascular disease. Mitophagy is a highly regulated and complex process that requires the coordination of labeling dysfunctional mitochondria for degradation while simultaneously promoting de novo autophagosome biogenesis adjacent to the cargo. In this review, we provide an update on our current understanding of these steps in mitophagy induction and discuss the physiological and pathophysiological consequences of altered mitophagy in the heart.

Indexed as

AnimalsCardiovascular DiseasesCardiovascular SystemCOVID-19HumansMitochondriaMitophagyPhagocytosisReactive Oxygen SpeciesReactive Oxygen SpeciesautophagyCOVID-19heartmitochondriamitophagy

Identifiers

PMID34965154
PMCPMC8816617
OpenAlexW4200297856

What Socratic holds

Textmetadata
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 Socratic graph.