Evidence map›Paper›PMID 31944918›Full record

ReviewCirculation research2020

Role of Mitochondrial Calcium and the Permeability Transition Pore in Regulating Cell Death.

Tyler M Bauer, Elizabeth Murphy

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 233 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
233citing papers in PubMed, 1 pooled it
18.7field-weighted citation impact, top 1% 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

233 citing papers in PubMed, 1 synthesis or guideline pooled it, 431 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Mechanistic Modeling of MCUx Gatekeeping, CaAmerican journal of physiology. Cell physiology · 2026
    Article
  8. Review
  9. Mercury-induced excitotoxicity in autism spectrum disorder: disruption of glutamatergic homeostasis and the therapeutic role of the selenium-glutathione axis.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Review
  10. Review
  11. Network pharmacology reveals thatGenes & diseases · 2026
    Article
  12. Sex differences in mitochondrial CaJournal of molecular and cellular cardiology · 2026
    Article
  13. Article
  14. Article
  15. Article
  16. CypD Dependent mPTP Opening Is Crucial for Oxidized Mitochondrial DNA Release in Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  17. Review
  18. Review
  19. Mitochondria-associated programmed cell death in pancreatic β cell of T2DM.Apoptosis : an international journal on programmed cell death · 2026
    Review
  20. Review

173 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 at 1 institution in 1 country.

Tyler M BauerLaboratory of Cardiac Physiology, National Heart, Lung and Blood Institute, Bethesda, MD.
Elizabeth MurphyLaboratory of Cardiac Physiology, National Heart, Lung and Blood Institute, Bethesda, MD.
National Heart Lung and Blood Institute · US

Funding

Mechanisms of cardiac ischemia-reperfusion injury and cardioprotectionZIAHL002066 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI MURPHY, ELIZABETH · 2009 to 2025
$20.4M
Role of S-nitrosylation in regulating cardiac function and diseaseZIAHL006059 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI MURPHY, ELIZABETH · 2010 to 2025
$7.2M
Mechanisms of cardiac ischemia-reperfusion injury and cardioprotectionZ01HL002066 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI MURPHY, ELIZABETH · 2008 to 2008
$607k
Intramural NIH HHS Z01 HL002066Intramural NIH HHS ZIA HL002066Intramural NIH HHS ZIA HL006059
6 · The paper itself

Abstract

Adult cardiomyocytes are postmitotic cells that undergo very limited cell division. Thus, cardiomyocyte death as occurs during myocardial infarction has very detrimental consequences for the heart. Mitochondria have emerged as an important regulator of cardiovascular health and disease. Mitochondria are well established as bioenergetic hubs for generating ATP but have also been shown to regulate cell death pathways. Indeed many of the same signals used to regulate metabolism and ATP production, such as calcium and reactive oxygen species, are also key regulators of mitochondrial cell death pathways. It is widely hypothesized that an increase in calcium and reactive oxygen species activate a large conductance channel in the inner mitochondrial membrane known as the PTP (permeability transition pore) and that opening of this pore leads to necroptosis, a regulated form of necrotic cell death. Strategies to reduce PTP opening either by inhibition of PTP or inhibiting the rise in mitochondrial calcium or reactive oxygen species that activate PTP have been proposed. A major limitation of inhibiting the PTP is the lack of knowledge about the identity of the protein(s) that form the PTP and how they are activated by calcium and reactive oxygen species. This review will critically evaluate the candidates for the pore-forming unit of the PTP and discuss recent data suggesting that assumption that the PTP is formed by a single molecular identity may need to be reconsidered.

Indexed as

Cell DeathAnimalsCalciumHumansMitochondria, HeartMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreReactive Oxygen SpeciesCalciumMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreReactive Oxygen Speciescalciumcell deathmitochondriapermeabilityreactive oxygen species

Identifiers

PMID31944918
PMCPMC8317591
OpenAlexW3000062473

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.