Evidence map›Paper›PMID 21920313›Full record

ArticleDevelopmental cell2011

The permeability transition pore controls cardiac mitochondrial maturation and myocyte differentiation.

Jennifer R Hom, Rodrigo A Quintanilla, David L Hoffman, Karen L de Mesy Bentley, Jeffery D Molkentin, Shey-Shing Sheu, George A Porter

Erratum issuedOpen access · bronzeAbstract readComment
In one paragraph

Article in Developmental cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 190 papers.

0numbers the graph read from it
0cells of the map it votes in
190citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

190 citing papers in PubMed, 288 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Cyclophilin D at the Heart of Neonatal Hypoxia.JACC. Basic to translational science · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Mitochondrial Amount Determines Doxorubicin-Induced Cardiotoxicity in Cardiomyocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  17. RNA-binding proteins as versatile metabolic regulators.npj metabolic health and disease · 2025
    Article
  18. A Mitochondrial Basis for Heart Failure Progression.Cardiovascular drugs and therapy · 2024
    Review
  19. Article
  20. Article

130 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Jennifer R HomDepartment of Pediatrics Division of Cardiology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
Rodrigo A Quintanilla
David L Hoffman
Karen L de Mesy Bentley
Jeffery D Molkentin
Shey-Shing Sheu
George A Porter
University of Rochester · USCincinnati Children's Hospital Medical Center · USThomas Jefferson University · US

Funding

UNIVERSITY OF ROCHESTER'S RESEARCH ASSOCIATE ORGANIZATIONUL1RR024160 · NCRR · UNIVERSITY OF ROCHESTER · PI PEARSON, THOMAS ARTHUR · 2006 to 2011
$38.7M
Ca2+ and ROS Crosstalk Signaling in Cardiac MitochondriaR01HL093671 · NHLBI · UNIVERSITY OF ROCHESTER · PI SHEU, SHEY-SHING · 2010 to 2023
$5.1M
MYOCARDIAL CA2+ TRANSPORT AND METABOLISMR01HL033333 · NHLBI · UNIVERSITY OF ROCHESTER · PI SHEU, SHEY-SHING · 1985 to 2010
$2.3M
NCRR NIH HHS UL1 RR024160NHLBI NIH HHS R01 HL033333NHLBI NIH HHS R01HL033333NHLBI NIH HHS R01 HL093671NHLBI NIH HHS R01HL093671
6 · The paper itself

Abstract

Although mature myocytes rely on mitochondria as the primary source of energy, the role of mitochondria in the developing heart is not well known. Here, we find that closure of the mitochondrial permeability transition pore (mPTP) drives maturation of mitochondrial structure and function and myocyte differentiation. Cardiomyocytes at embryonic day (E) 9.5, when compared to E13.5, displayed fragmented mitochondria with few cristae, a less-polarized mitochondrial membrane potential, higher reactive oxygen species (ROS) levels, and an open mPTP. Pharmacologic and genetic closing of the mPTP yielded maturation of mitochondrial structure and function, lowered ROS, and increased myocyte differentiation (measured by counting Z bands). Furthermore, myocyte differentiation was inhibited and enhanced with oxidant and antioxidant treatment, respectively, suggesting that redox-signaling pathways lie downstream of mitochondria to regulate cardiac myocyte differentiation.

Identifiers

PMID21920313
PMCPMC3175092
OpenAlexW2082973248

What OpenQuestion holds

Textmetadata
LicenceTDM
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.