Evidence map›Paper›PMID 25323859›Full record

ReviewCirculation research2015

The mitochondrial dynamism-mitophagy-cell death interactome: multiple roles performed by members of a mitochondrial molecular ensemble.

Gerald W Dorn, Richard N Kitsis

Abstract readReview
In one paragraph

Review in Circulation research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing 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

110 citing papers in PubMed.

  1. Article
  2. Review
  3. METTL16-mBMC biology · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Mitochondrial Dysfunction in Cardiovascular Diseases.International journal of molecular sciences · 2025
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

50 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.

Gerald W DornFrom the Department of Internal Medicine, Center for Pharmacogenomics, Washington University School of Medicine, St. Louis, MO (G.W.D.); and Departments of Medicine (Cardiology) and Cell Biology and Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine, Bronx, NY (R.N.K.). gdorn@dom.wustl.edu.
Richard N KitsisFrom the Department of Internal Medicine, Center for Pharmacogenomics, Washington University School of Medicine, St. Louis, MO (G.W.D.); and Departments of Medicine (Cardiology) and Cell Biology and Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine, Bronx, NY (R.N.K.).

Funding

MOLECULAR MECHANISM OF APOPTOTIC CARDIOMYOPATHYR01HL059888 · NHLBI · WASHINGTON UNIVERSITY · PI DORN, GERALD W. · 1999 to 2016
$5.4M
CARDIAC MYOCYTE APOPTOSIS--MECHANISM AND SIGNIFICANCER01HL060665 · NHLBI · YESHIVA UNIVERSITY · PI KITSIS, RICHARD N · 1998 to 2013
$5.3M
NHLBI NIH HHS HL59888NHLBI NIH HHS HL60665NHLBI NIH HHS R01 HL059888NHLBI NIH HHS R01 HL060665
6 · The paper itself

Abstract

Mitochondrial research is experiencing a renaissance, in part, because of the recognition that these endosymbiotic descendants of primordial protobacteria seem to be pursuing their own biological agendas. Not only is mitochondrial metabolism required to produce most of the biochemical energy that supports their eukaryotic hosts (us) but mitochondria can actively (through apoptosis and programmed necrosis) or passively (through reactive oxygen species toxicity) drive cellular dysfunction or demise. The cellular mitochondrial collective autoregulates its population through biogenic renewal and mitophagic culling; mitochondrial fission and fusion, 2 components of mitochondrial dynamism, are increasingly recognized as playing central roles as orchestrators of these processes. Mitochondrial dynamism is rare in striated muscle cells, so cardiac-specific genetic manipulation of mitochondrial fission and fusion factors has proven useful for revealing noncanonical functions of mitochondrial dynamics proteins. Here, we review newly described functions of mitochondrial fusion/fission proteins in cardiac mitochondrial quality control, cell death, calcium signaling, and cardiac development. A mechanistic conceptual paradigm is proposed in which cell death and selective organelle culling are not distinct processes, but are components of a unified and integrated quality control mechanism that exerts different effects when invoked to different degrees, depending on pathophysiological context. This offers a plausible explanation for seemingly paradoxical expression of mitochondrial dynamics and death factors in cardiomyocytes wherein mitochondrial morphometric remodeling does not normally occur and the ability to recover from cell suicide is severely limited.

Indexed as

AnimalsCell DeathHumansMitochondria, HeartMitochondrial DynamicsMitophagyapoptosisautophagymitochondriamitochondrial dynamics

Identifiers

PMID25323859
PMCPMC4282600

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Registered trials

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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.