Evidence map›Paper›PMID 25252178›Full record

ArticleJournal of molecular and cellular cardiology2014

Regulation of metabolism in individual mitochondria during excitation-contraction coupling.

Guohua Gong, Xiaoyun Liu, Wang Wang

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

27 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Mitochondrial CaInternational journal of molecular sciences · 2022
    Review
  6. Review
  7. Review
  8. Mitochondrial calcium uniporter complex activation protects against calcium alternans in atrial myocytes.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  9. Article
  10. Why don't mice lacking the mitochondrial CaThe Journal of physiology · 2020
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Role of mitochondrial CaArchives of biochemistry and biophysics · 2019
    Review
  18. Article
  19. Article
  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

3 authors at 2 institutions in 2 countries.

Guohua GongMitochondria and Metabolism Center, Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA 98109, USA.
Xiaoyun LiuMitochondria and Metabolism Center, Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA 98109, USA; Department of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China.
Wang WangMitochondria and Metabolism Center, Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA 98109, USA. Electronic address: wangwang@u.washington.edu.
University of Washington · USSecond Hospital of Hebei Medical University · CN

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Karin E Bornfeldt · 1986 to 2026
$41.4M
NAD+/NADH ratio, protein acetylation and mitochondrial functionR01HL110349 · NHLBI · UNIVERSITY OF WASHINGTON · PI TIAN, RONG · 2011 to 2020
$5.7M
Mitochondrial Respiration and Superoxide Production in Healthy and Failing HeartR01HL114760 · NHLBI · UNIVERSITY OF WASHINGTON · PI WANG, WANG · 2012 to 2016
$2.1M
NHLBI NIH HHS HL110349NHLBI NIH HHS HL114760NHLBI NIH HHS R01 HL110349NHLBI NIH HHS R01 HL114760NIDDK NIH HHS P30 DK017047
6 · The paper itself

Abstract

The heart is an excitable organ that undergoes spontaneous force generation and relaxation cycles driven by excitation-contraction (EC) coupling. A fraction of the oscillating cytosolic Ca(2+) during each heartbeat is taken up by mitochondria to stimulate mitochondrial metabolism, the major source of energy in the heart. Whether the mitochondrial metabolism is regulated individually during EC coupling and whether this heterogeneous regulation bears any physiological or pathological relevance have not been studied. Here, we developed a novel approach to determine the regulation of individual mitochondrial metabolism during cardiac EC coupling. Through monitoring superoxide flashes, which are stochastic and bursting superoxide production events arising from increased metabolism in individual mitochondria, we found that EC coupling stimulated the metabolism in individual mitochondria as indicated by significantly increased superoxide flash activity during electrical stimulation of the cultured intact myocytes or perfused heart. Mechanistically, cytosolic calcium transients promoted individual mitochondria to take up calcium via mitochondrial calcium uniporter, which subsequently triggered transient opening of the permeability transition pore and stimulated metabolism and bursting superoxide flash in that mitochondrion. The bursting superoxide, in turn, promoted local calcium release. In the early stage of heart failure, EC coupling regulation of superoxide flashes was compromised. This study highlights the heterogeneity in the regulation of cardiac mitochondrial metabolism, which may contribute to local redox signaling.

Indexed as

Excitation Contraction CouplingAnimalsCells, CulturedEnergy MetabolismFemaleHeart FailureHEK293 CellsHumansMice, TransgenicMitochondria, HeartMyocytes, CardiacRats, Sprague-DawleyExcitation–contraction couplingMitochondrial calcium uptakeMitochondrial metabolismPermeability transition poreSuperoxide flash

Identifiers

PMID25252178
PMCPMC4250349
OpenAlexW2122046060

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.