Evidence map›Paper›PMID 19161975›Full record

ReviewBiochimica et biophysica acta2009

Characteristics and possible functions of mitochondrial Ca(2+) transport mechanisms.

Thomas E Gunter, Shey-Shing Sheu

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed
9.0field-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

113 citing papers in PubMed, 216 citations in OpenAlex.

  1. Trial
  2. Review
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  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Mitochondrial CaInternational journal of molecular sciences · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Mitochondrial Calcification.Immunometabolism · 2021
    Article

53 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 2 institutions in 1 country.

Thomas E GunterDepartment of Biochemistry and Biophysics and Mitochondrial Research and Innovation Group, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Rochester, NY 14642, USA. Thomas_gunter@urmc.rochester.edu
Shey-Shing Sheu
University of Rochester · USUniversity of Rochester Medical Center · US

Funding

Ca2+ and ROS Crosstalk Signaling in Cardiac MitochondriaR01HL093671 · NHLBI · UNIVERSITY OF ROCHESTER · PI SHEU, SHEY-SHING · 2010 to 2023
$5.1M
Mitochondrial Role in Manganese ToxicityR01ES010041 · NIEHS · UNIVERSITY OF ROCHESTER · PI GUNTER, THOMAS · 2000 to 2010
$3.1M
MYOCARDIAL CA2+ TRANSPORT AND METABOLISMR01HL033333 · NHLBI · UNIVERSITY OF ROCHESTER · PI SHEU, SHEY-SHING · 1985 to 2010
$2.3M
NHLBI NIH HHS HL 33333NHLBI NIH HHS R01 HL033333NHLBI NIH HHS R01 HL093671NIEHS NIH HHS R01 ES010041NIEHS NIH HHS R01 ES10041
6 · The paper itself

Abstract

Mitochondria produce around 92% of the ATP used in the typical animal cell by oxidative phosphorylation using energy from their electrochemical proton gradient. Intramitochondrial free Ca(2+) concentration ([Ca(2+)](m)) has been found to be an important component of control of the rate of this ATP production. In addition, [Ca(2+)](m) also controls the opening of a large pore in the inner mitochondrial membrane, the permeability transition pore (PTP), which plays a role in mitochondrial control of programmed cell death or apoptosis. Therefore, [Ca(2+)](m) can control whether the cell has sufficient ATP to fulfill its functions and survive or is condemned to death. Ca(2+) is also one of the most important second messengers within the cytosol, signaling changes in cellular response through Ca(2+) pulses or transients. Mitochondria can also sequester Ca(2+) from these transients so as to modify the shape of Ca(2+) signaling transients or control their location within the cell. All of this is controlled by the action of four or five mitochondrial Ca(2+) transport mechanisms and the PTP. The characteristics of these mechanisms of Ca(2+) transport and a discussion of how they might function are described in this paper.

Indexed as

AnimalsCalciumHumansIon TransportMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreReactive Oxygen SpeciesRyanodine Receptor Calcium Release ChannelSodiumCalciumMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreReactive Oxygen SpeciesRyanodine Receptor Calcium Release ChannelSodium

Identifiers

PMID19161975
PMCPMC2730425
OpenAlexW2115448092

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.