Evidence map›Paper›PMID 19162034›Full record

ArticleJournal of molecular and cellular cardiology2009

Mitochondrial Ca2+ uptake: tortoise or hare?

Brian O'Rourke, Lothar A Blatter

Abstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing 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

73 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. CaBiomolecules · 2025
    Review
  5. Review
  6. Article
  7. MICU1 and MICU2 control mitochondrial calcium signaling in the mammalian heart.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. MCU overexpression evokes disparate dose-dependent effects on mito-ROS and spontaneous CaAmerican journal of physiology. Heart and circulatory physiology · 2021
    Article
  15. Mitochondrial CaCells · 2021
    Review
  16. Review
  17. Excitation-contraction coupling and calcium release in atrial muscle.Pflugers Archiv : European journal of physiology · 2021
    Review
  18. Regulation of Mitochondrial CaAnnual review of physiology · 2021
    Review
  19. Review
  20. Mitochondrial calcium uniporter complex activation protects against calcium alternans in atrial myocytes.American journal of physiology. Heart and circulatory physiology · 2020
    Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Brian O'RourkeDepartment of Medicine, Division of Cardiology, Johns Hopkins University, Institute of Molecular Cardiobiology, Baltimore, MD 21205-2195, USA. bor@jhmi.edu
Lothar A Blatter

Funding

Program AdministrationP01HL080101 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERS, DONALD M · 2006 to 2015
$23.4M
STRUCTURE OF MITOCHONDRIAL K+ CHANNELSP01HL081427 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI VAN EYK, JENNIFER E · 2005 to 2009
$11.2M
E/C COUPLING AND CALCIUM REGULATION IN ATRIAL MYOCYTESR01HL062231 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI BLATTER, LOTHAR A · 1999 to 2012
$4.4M
MItochondrial Dysfunction in Cardiac Hypertrophy and FailureR01HL101235 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BERS, DONALD M, BLATTER, LOTHAR A · 2010 to 2013
$2.8M
NHLBI NIH HHS P01 HL080101NHLBI NIH HHS P01 HL081427NHLBI NIH HHS R01 HL062231NHLBI NIH HHS R01 HL101235
6 · The paper itself

Abstract

Mitochondria are equipped with an efficient machinery for Ca(2+) uptake and extrusion and are capable of storing large amounts of Ca(2+). Furthermore, key steps of mitochondrial metabolism (ATP production) are Ca(2+)-dependent. In the field of cardiac physiology and pathophysiology, two main questions have dominated the thinking about mitochondrial function in the heart: 1) how does mitochondrial Ca(2+) buffering shape cytosolic Ca(2+) levels and affect excitation-contraction coupling, particularly the Ca(2+) transient, on a beat-to-beat basis, and 2) how does mitochondrial Ca(2+) homeostasis influence cardiac energy metabolism. To answer these questions, a thorough understanding of the kinetics of mitochondrial Ca(2+) transport and buffer capacity is required. Here, we summarize the role of mitochondrial Ca(2+) signaling in the heart, discuss the evidence either supporting or arguing against the idea that Ca(2+) can be taken up rapidly by mitochondria during excitation-contraction coupling and highlight some interesting new areas for further investigation.

Indexed as

AnimalsBiological TransportCalciumCalcium SignalingEnergy MetabolismHumansMitochondriaMitochondrial MembranesSodiumCalciumSodium

Identifiers

PMID19162034
PMCPMC4005816

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.