Evidence map›Paper›PMID 30540226›Full record

ReviewPhysiological reviews2019

Evolving and Expanding the Roles of Mitophagy as a Homeostatic and Pathogenic Process.

Åsa B Gustafsson, Gerald W Dorn

Abstract readReview
In one paragraph

Review in Physiological reviews, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed, 1 pooled it
–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

140 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. APurinergic signalling · 2026
    Article
  13. MTFR1L is a cardiac antiaging factor for maintenance of mitochondrial homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Mitophagy: a novel avenue for herbal medicines alleviating myocardial ischemia/reperfusion injury.Apoptosis : an international journal on programmed cell death · 2025
    Review
  20. Article

80 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

2 authors.

Åsa B GustafssonSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California San Diego , La Jolla, California ; and Washington University School of Medicine, St. Louis, Missouri.
Gerald W DornSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California San Diego , La Jolla, California ; and Washington University School of Medicine, St. Louis, Missouri.

Funding

Surgery, Physiology and ImmunohistopathologyP01HL085577 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI GUSTAFSSON, ASA B. · 2006 to 2017
$18.4M
THE MITOCHONDRIAL DYNAMISM/FITNESS/BIOGENESIS INTERACTOME IN CARDIAC DISEASER35HL135736 · NHLBI · WASHINGTON UNIVERSITY · PI DORN, GERALD W. · 2017 to 2023
$6.4M
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
Mitochondrial Quality Control in the Aging MyocardiumR21AG052280 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUSTAFSSON, ASA B. · 2016 to 2017
$426k
NHLBI NIH HHS P01 HL085577NHLBI NIH HHS R01 HL132300NHLBI NIH HHS R01 HL138560NHLBI NIH HHS R35 HL135736NIA NIH HHS R21 AG052280
6 · The paper itself

Abstract

The central functions fulfilled by mitochondria as both energy generators essential for tissue homeostasis and gateways to programmed apoptotic and necrotic cell death mandate tight control over the quality and quantity of these ubiquitous endosymbiotic organelles. Mitophagy, the targeted engulfment and destruction of mitochondria by the cellular autophagy apparatus, has conventionally been considered as the mechanism primarily responsible for mitochondrial quality control. However, our understanding of how, why, and under what specific conditions mitophagy is activated has grown tremendously over the past decade. Evidence is accumulating that nonmitophagic mitochondrial quality control mechanisms are more important to maintaining normal tissue homeostasis whereas mitophagy is an acute tissue stress response. Moreover, previously unrecognized mitophagic regulation of mitochondrial quantity control, metabolic reprogramming, and cell differentiation suggests that the mechanisms linking genetic or acquired defects in mitophagy to neurodegenerative and cardiovascular diseases or cancer are more complex than simple failure of normal mitochondrial quality control. Here, we provide a comprehensive overview of mitophagy in cellular homeostasis and disease and examine the most revolutionary concepts in these areas. In this context, we discuss evidence that atypical mitophagy and nonmitophagic pathways play central roles in mitochondrial quality control, functioning that was previously considered to be the primary domain of mitophagy.

Indexed as

AnimalsAutophagyCell DifferentiationHomeostasisHumansMitochondriaMitophagyNeoplasms

Identifiers

PMID30540226
PMCPMC6442924

What OpenQuestion 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 OpenQuestion graph.