Evidence map›Paper›PMID 38157298›Full record

ArticleCell reports2024

CHCHD4-TRIAP1 regulation of innate immune signaling mediates skeletal muscle adaptation to exercise.

Jin Ma, Ping-Yuan Wang, Jie Zhuang, Annie Y Son, Alexander K Karius, Abu Mohammad Syed, Masahiro Nishi, Zhichao Wu, Mateus P Mori, Young-Chae Kim and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
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  3. cGAS: bridging immunity and metabolic regulation.Journal of molecular cell biology · 2026
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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

11 authors at 2 institutions in 2 countries.

Jin MaCardiovascular Branch, National Heart, Lung, and Blood Institute (NHLBI), NIH, Bethesda, MD 20892, USA.
Ping-Yuan WangCardiovascular Branch, National Heart, Lung, and Blood Institute (NHLBI), NIH, Bethesda, MD 20892, USA.
Jie ZhuangCardiovascular Branch, National Heart, Lung, and Blood Institute (NHLBI), NIH, Bethesda, MD 20892, USA; School of Medicine, Nankai University, Tianjin 300071, China.
Annie Y SonCardiovascular Branch, National Heart, Lung, and Blood Institute (NHLBI), NIH, Bethesda, MD 20892, USA.
Alexander K KariusCardiovascular Branch, National Heart, Lung, and Blood Institute (NHLBI), NIH, Bethesda, MD 20892, USA.
Abu Mohammad SyedCardiovascular Branch, National Heart, Lung, and Blood Institute (NHLBI), NIH, Bethesda, MD 20892, USA.
Masahiro NishiCardiovascular Branch, National Heart, Lung, and Blood Institute (NHLBI), NIH, Bethesda, MD 20892, USA.
Zhichao WuLaboratory of Pathology, National Cancer Institute (NCI), NIH, Bethesda, MD 20892, USA.
Mateus P MoriCardiovascular Branch, National Heart, Lung, and Blood Institute (NHLBI), NIH, Bethesda, MD 20892, USA.
Young-Chae KimCardiovascular Branch, National Heart, Lung, and Blood Institute (NHLBI), NIH, Bethesda, MD 20892, USA.
Paul M HwangCardiovascular Branch, National Heart, Lung, and Blood Institute (NHLBI), NIH, Bethesda, MD 20892, USA. Electronic address: hwangp@mail.nih.gov.
National Heart Lung and Blood Institute · USNational Cancer Institute · US

Funding

Redox homeostasis in cancer and cardiovascular diseasesZIAHL006051 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI HWANG, PAUL M. · 2010 to 2025
$12.8M
Intramural NIH HHS ZIA HL006051
6 · The paper itself

Abstract

Exercise training can stimulate the formation of fatty-acid-oxidizing slow-twitch skeletal muscle fibers, which are inversely correlated with obesity, but the molecular mechanism underlying this transformation requires further elucidation. Here, we report that the downregulation of the mitochondrial disulfide relay carrier CHCHD4 by exercise training decreases the import of TP53-regulated inhibitor of apoptosis 1 (TRIAP1) into mitochondria, which can reduce cardiolipin levels and promote VDAC oligomerization in skeletal muscle. VDAC oligomerization, known to facilitate mtDNA release, can activate cGAS-STING/NFKB innate immune signaling and downregulate MyoD in skeletal muscle, thereby promoting the formation of oxidative slow-twitch fibers. In mice, CHCHD4 haploinsufficiency is sufficient to activate this pathway, leading to increased oxidative muscle fibers and decreased fat accumulation with aging. The identification of a specific mediator regulating muscle fiber transformation provides an opportunity to understand further the molecular underpinnings of complex metabolic conditions such as obesity and could have therapeutic implications.

Indexed as

Muscle Fibers, SkeletalMuscle, SkeletalAnimalsApoptosisImmunity, InnateMiceMitochondrial Precursor Protein Import Complex ProteinsObesityChchd4 protein, mouseMitochondrial Precursor Protein Import Complex ProteinscardiolipinCHCHD4CP: Immunologyexercise adaptationinnate immune signalingmitochondriamtDNAMyoDskeletal muscleTRIAP1VDAC

Identifiers

PMID38157298
PMCPMC10851177
OpenAlexW4390379152

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.