Evidence map›Paper›PMID 20847324›Full record

ReviewCirculation research2010

Two close, too close: sarcoplasmic reticulum-mitochondrial crosstalk and cardiomyocyte fate.

Gerald W Dorn, Luca Scorrano

Abstract readReview
In one paragraph

Review in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing 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

41 citing papers in PubMed.

  1. Article
  2. Oxidative Stress and Its Role in Vascular Damage and Atherosclerosis.International journal of molecular sciences · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Neurohormonal connections with mitochondria in cardiomyopathy and other diseases.American journal of physiology. Cell physiology · 2022
    Review
  9. Article
  10. Targeting mitochondrial fusion and fission proteins for cardioprotection.Journal of cellular and molecular medicine · 2020
    Review
  11. Mitochondrial adventures at the organelle society.Biochemical and biophysical research communications · 2018
    Review
  12. Pharmacological Modulation of Mitochondrial CaFrontiers in physiology · 2018
    Article
  13. Mitochondria and Reactive Oxygen Species in Aging and Age-Related Diseases.International review of cell and molecular biology · 2018
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. The mitochondrial function of the cerebral vasculature in insulin-resistant Zucker obese rats.American journal of physiology. Heart and circulatory physiology · 2016
    Article
  19. Review
  20. Article
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 DornWashington University Center for Pharmacogenomics, Campus Box 8220, 660 S Euclid Ave, St Louis, MO 63110, USA. gdorn@dom.wustl.edu
Luca Scorrano

Funding

MOLECULAR MECHANISM OF APOPTOTIC CARDIOMYOPATHYR01HL059888 · NHLBI · WASHINGTON UNIVERSITY · PI DORN, GERALD W. · 1999 to 2016
$5.4M
G-Protein Receptor Kinases in Cardiac Stress AdaptationR01HL087871 · NHLBI · WASHINGTON UNIVERSITY · PI DORN, GERALD W. · 2007 to 2016
$4.1M
CTRIP: Genetic Testing to Individualize Management of Common Heart DiseasesRC2HL102222 · NHLBI · WASHINGTON UNIVERSITY · PI DORN, GERALD W. · 2009 to 2010
$1.9M
Calpains as Mediators of Cardiac Ischemic InjuryR01HL080008 · NHLBI · WASHINGTON UNIVERSITY · PI DORN, GERALD W. · 2006 to 2010
$1.9M
NHLBI NIH HHS R01 HL059888NHLBI NIH HHS R01 HL080008NHLBI NIH HHS R01 HL087871NHLBI NIH HHS RC2 HL102222Telethon GGP06254
6 · The paper itself

Abstract

Mitochondria are key organelles in cell life whose dysfunction is associated with a variety of diseases. Their crucial role in intermediary metabolism and energy conversion makes them a preferred target in tissues, such as the heart, where the energetic demands are very high. In the cardiomyocyte, the spatial organization of mitochondria favors their interaction with the sarcoplasmic reticulum, thereby offering a mechanism for Ca(2+)-mediated crosstalk between these 2 organelles. Recently, the molecular basis for this interaction has begun to be unraveled, and we are learning how endoplasmic reticulum-mitochondrial interactions are often exploited by death signals, such as proapoptotic Bcl-2 family members, to amplify the cell death cascade. Here, we review our present understanding of the structural basis and the functional consequences of the close interaction between sarcoplasmic reticulum and mitochondria on cardiomyocyte function and death.

Indexed as

AnimalsCell CommunicationHumansMitochondria, HeartMyocytes, CardiacSarcoplasmic Reticulum

Identifiers

PMID20847324
PMCPMC2963937

What OpenQuestion holds

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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.