Evidence map›Paper›PMID 37641565›Full record

ReviewBiochemical Society transactions2023

Beyond the TCA cycle: new insights into mitochondrial calcium regulation of oxidative phosphorylation.

Sandra H Lee, Hannah E Duron, Dipayan Chaudhuri

Open access · greenAbstract readReview
In one paragraph

Review in Biochemical Society transactions, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
8.6field-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

43 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. The two faces of mitochondrial CaJournal of physiology and biochemistry · 2026
    Review
  8. TRPV6-Mediated CaCancers · 2026
    Review
  9. Article
  10. Mitochondrial Calcium Signaling in Hepatocyte Health and Disease.Cold Spring Harbor perspectives in biology · 2026
    Review
  11. Article
  12. Fuelling the brain with calcium.Nature metabolism · 2026
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Peroxynitrite regulates ER stress-mediated CaJournal of translational medicine · 2025
    Article
  18. HIFU-Driven Targeted Pyroptosis Therapy in Basal-Like Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    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 1 institution in 1 country.

Sandra H LeeNora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, Utah, U.S.A.
Hannah E DuronNora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, Utah, U.S.A.
Dipayan ChaudhuriNora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, Utah, U.S.A.ORCID 0000-0003-0605-7334
University of Utah · US

Funding

Metabolic Impact and Mechanism of Enhanced Mitochondrial Calcium Uptake in Mitochondrial CardiomyopathiesR01HL141353 · NHLBI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Dipayan Chaudhuri · 2018 to 2026
$4.3M
Regulation of the mitochondrial calcium uniporterR01HL165797 · NHLBI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Dipayan Chaudhuri · 2022 to 2026
$2.5M
Structural basis for mitochondrial calcium uniporter functionR00HL124070 · NHLBI · UNIVERSITY OF UTAH · PI CHAUDHURI, DIPAYAN · 2016 to 2018
$747k
Structural basis for mitochondrial calcium uniporter functionK99HL124070 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHAUDHURI, DIPAYAN · 2014 to 2015
$292k
A novel mechanism of mitochondrial protein turnover in Complex I deficient mitochondrial cardiomyopathyF30HL165806 · NHLBI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI CVRTI, SANDRA HYUNJOO · 2022 to 2025
$169k
NHLBI NIH HHS F30 HL165806NHLBI NIH HHS K99 HL124070NHLBI NIH HHS R00 HL124070NHLBI NIH HHS R01 HL141353NHLBI NIH HHS R01 HL165797
6 · The paper itself

Abstract

While mitochondria oxidative phosphorylation is broadly regulated, the impact of mitochondrial Ca2+ on substrate flux under both physiological and pathological conditions is increasingly being recognized. Under physiologic conditions, mitochondrial Ca2+ enters through the mitochondrial Ca2+ uniporter and boosts ATP production. However, maintaining Ca2+ homeostasis is crucial as too little Ca2+ inhibits adaptation to stress and Ca2+ overload can trigger cell death. In this review, we discuss new insights obtained over the past several years expanding the relationship between mitochondrial Ca2+ and oxidative phosphorylation, with most data obtained from heart, liver, or skeletal muscle. Two new themes are emerging. First, beyond boosting ATP synthesis, Ca2+ appears to be a critical determinant of fuel substrate choice between glucose and fatty acids. Second, Ca2+ exerts local effects on the electron transport chain indirectly, not via traditional allosteric mechanisms. These depend critically on the transporters involved, such as the uniporter or the Na+-Ca2+ exchanger. Alteration of these new relationships during disease can be either compensatory or harmful and suggest that targeting mitochondrial Ca2+ may be of therapeutic benefit during diseases featuring impairments in oxidative phosphorylation.

Indexed as

CalciumOxidative PhosphorylationAdenosine TriphosphateCell DeathMitochondriaAdenosine TriphosphateCalciumelectron transport chainMCUmitochondrial dysfunctionmitochondrial permeability transition poresNCLXoxidative phosphorylation

Identifiers

PMID37641565
PMCPMC10508640
OpenAlexW4386252322

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.