Evidence map›Paper›PMID 32017711›Full record

ArticleJCI insight2020

EMRE is essential for mitochondrial calcium uniporter activity in a mouse model.

Julia C Liu, Nicole C Syder, Nima S Ghorashi, Thomas B Willingham, Randi J Parks, Junhui Sun, Maria M Fergusson, Jie Liu, Kira M Holmström, Sara Menazza and 5 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
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

45 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Perturbation of mitochondrial CaStress biology · 2026
    Article
  3. Article
  4. Sex differences in mitochondrial CaJournal of molecular and cellular cardiology · 2026
    Article
  5. Phenotypic CRISPR screens identify NLRX1 as an essential activator of the human mitochondrial permeability transition.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. MCU-independent CaScientific reports · 2024
    Article
  18. Mechanisms of reduced myocardial energetics of the dystrophic heart.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  19. Article
  20. Loss of mitochondrial CaThe Journal of physiology · 2024
    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

15 authors at 2 institutions in 1 country.

Julia C LiuCardiovascular Branch and.
Nicole C SyderCardiovascular Branch and.
Nima S GhorashiCardiovascular Branch and.
Thomas B WillinghamSystems Biology Center, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, USA.
Randi J ParksCardiovascular Branch and.
Junhui SunCardiovascular Branch and.
Maria M FergussonCardiovascular Branch and.
Jie LiuCenter for Molecular Medicine, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, USA.
Kira M HolmströmCenter for Molecular Medicine, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, USA.
Sara MenazzaCardiovascular Branch and.
Danielle A SpringerMurine Phenotyping Core and.
Chengyu LiuTransgenic Core, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, USA.
Brian GlancySystems Biology Center, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, USA.
Toren FinkelCenter for Molecular Medicine, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, USA.
Elizabeth MurphyCardiovascular Branch and.
National Heart Lung and Blood Institute · USNational Institute of Arthritis and Musculoskeletal and Skin Diseases · US

Funding

Transgenic CoreZICHL005907 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI LIU, CHENGYU · 2010 to 2025
$25.8M
Mechanisms of cardiac ischemia-reperfusion injury and cardioprotectionZIAHL002066 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI MURPHY, ELIZABETH · 2009 to 2025
$20.4M
Murine Phenotyping CoreZIGHL006190 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI SPRINGER, DANIELLE · 2014 to 2025
$15.2M
Development and Regulation of the Muscle Mitochondrial ReticulumZIAHL006221 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI GLANCY, BRIAN · 2017 to 2025
$14.7M
The role of calcium entry through the mitochondrial uniporter in regulating cardiac metabolism and physiologyR01HL142589 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FINKEL, TOREN · 2019 to 2022
$2.6M
Molecular mechanism and physiological function of mitochondrial calcium regulationK22HL137901 · NHLBI · UNIVERSITY OF MINNESOTA · PI LIU, JULIA CHANG · 2020 to 2022
$747k
Molecular and physiological analysis of mitochondrial calcium uptakeFI2GM117605 · NIGMS · U.S. NATIONAL HEART LUNG AND BLOOD INST · PI LIU, JULIA CHANG · 2016 to 2016
–
NHLBI NIH HHS K22 HL137901NHLBI NIH HHS R01 HL142589NIGMS NIH HHS FI2 GM117605
6 · The paper itself

Abstract

The mitochondrial calcium uniporter is widely accepted as the primary route of rapid calcium entry into mitochondria, where increases in matrix calcium contribute to bioenergetics but also mitochondrial permeability and cell death. Hence, regulation of uniporter activity is critical to mitochondrial homeostasis. The uniporter subunit EMRE is known to be an essential regulator of the channel-forming protein MCU in cell culture, but EMRE's impact on organismal physiology is less understood. Here we characterize a mouse model of EMRE deletion and show that EMRE is indeed required for mitochondrial calcium uniporter function in vivo. EMRE-/- mice are born less frequently; however, the mice that are born are viable, healthy, and do not manifest overt metabolic impairment, at rest or with exercise. Finally, to investigate the role of EMRE in disease processes, we examine the effects of EMRE deletion in a muscular dystrophy model associated with mitochondrial calcium overload.

Indexed as

AnimalsCalciumCalcium ChannelsDisease Models, AnimalHeartMiceMice, KnockoutMitochondriaMitochondrial Membrane Transport ProteinsMyocardial Reperfusion InjuryCalciumCalcium Channelsmitochondrial calcium uniporterMitochondrial Membrane Transport ProteinsBioenergeticsCalciumCardiologyMitochondriaMuscle Biology

Identifiers

PMID32017711
PMCPMC7101141
OpenAlexW3005339179

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.