Evidence map›Paper›PMID 30429366›Full record

ArticleJCI insight2018

The mitochondrial calcium uniporter underlies metabolic fuel preference in skeletal muscle.

Jennifer Q Kwong, Jiuzhou Huo, Michael J Bround, Justin G Boyer, Jennifer A Schwanekamp, Nasab Ghazal, Joshua T Maxwell, Young C Jang, Zaza Khuchua, Kevin Shi and 3 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 6% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
  2. Elevated mitochondrial CaStem cell reports · 2026
    Article
  3. Article
  4. Molecular Framework of the Onset and Progression of Skeletal Muscle Aging.International journal of molecular sciences · 2025
    Review
  5. A fixed mutation in the respiratory complex I impairs mitochondrial bioenergetics in the endangered Apennine brown bear.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Article
  7. Mitochondrial CaJournal of cellular physiology · 2025
    Review
  8. Article
  9. Article
  10. Review
  11. Analyzing Mitochondrial Calcium Influx in Isolated Mitochondria.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  12. Article
  13. Article
  14. MCU genetically altered mice suggest how mitochondrial CaTrends in endocrinology and metabolism: TEM · 2024
    Review
  15. Review
  16. MCU-independent CaScientific reports · 2024
    Article
  17. Article
  18. Article
  19. Microcirculation and Mitochondria: The Critical Unit.Journal of clinical medicine · 2023
    Review
  20. Review
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

13 authors at 5 institutions in 2 countries.

Jennifer Q KwongDepartment of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, USA.
Jiuzhou HuoDepartment of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, USA.
Michael J BroundDepartment of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, USA.
Justin G BoyerDepartment of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, USA.
Jennifer A SchwanekampDepartment of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, USA.
Nasab GhazalDepartment of Pediatrics, Division of Cardiovascular Biology, Emory University School of Medicine, Atlanta, Georgia, USA.
Joshua T MaxwellDepartment of Pediatrics, Division of Cardiovascular Biology, Emory University School of Medicine, Atlanta, Georgia, USA.
Young C JangSchool of Biological Sciences, Georgia Institute of Technology, Atlanta, Georgia, USA.
Zaza KhuchuaDepartment of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, USA.
Kevin ShiDepartment of Bioengineering, University of Washington, Seattle, Washington, USA.
Donald M BersDepartment of Pharmacology, University of California, Davis, California, USA.
Jennifer DavisDepartment of Bioengineering, University of Washington, Seattle, Washington, USA.
Jeffery D MolkentinDepartment of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, Ohio, USA.
Cincinnati Children's Hospital Medical Center · USEmory University · USUniversity of Washington · USGeorgia Institute of Technology · USUniversity of California, Davis · US

Funding

Molecular examination of mitochondrial calcium controlR01HL132831 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI BERS, DONALD M, MOLKENTIN, JEFFERY D · 2016 to 2024
$5.9M
IONIC CONTROL OF CARDIAC MUSCLE CONTRACTION: EC COUPLINGR01HL030077 · NHLBI · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI BERS, DONALD M · 1986 to 2018
$3.8M
Howard Hughes Medical InstituteNHLBI NIH HHS R01 HL030077NHLBI NIH HHS R01 HL132831
6 · The paper itself

Abstract

The mitochondrial Ca2+ uniporter (MCU) complex mediates acute mitochondrial Ca2+ influx. In skeletal muscle, MCU links Ca2+ signaling to energy production by directly enhancing the activity of key metabolic enzymes in the mitochondria. Here, we examined the role of MCU in skeletal muscle development and metabolic function by generating mouse models for the targeted deletion of Mcu in embryonic, postnatal, and adult skeletal muscle. Loss of Mcu did not affect muscle growth and maturation or otherwise cause pathology. Skeletal muscle-specific deletion of Mcu in mice also did not affect myofiber intracellular Ca2+ handling, but it did inhibit acute mitochondrial Ca2+ influx and mitochondrial respiration stimulated by Ca2+, resulting in reduced acute exercise performance in mice. However, loss of Mcu also resulted in enhanced muscle performance under conditions of fatigue, with a preferential shift toward fatty acid metabolism, resulting in reduced body fat with aging. Together, these results demonstrate that MCU-mediated mitochondrial Ca2+ regulation underlies skeletal muscle fuel selection at baseline and under enhanced physiological demands, which affects total homeostatic metabolism.

Indexed as

AnimalsCalciumCalcium ChannelsCalcium SignalingEnergy MetabolismFemaleGene TargetingMaleMiceMice, TransgenicMuscle, SkeletalCalciumCalcium Channelsmitochondrial calcium uniporterCalciumCardiologyMitochondriaMuscle Biology

Identifiers

PMID30429366
PMCPMC6302934
OpenAlexW2901586290

What OpenQuestion holds

Textmetadata
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.