Evidence map›Paper›PMID 40237439›Full record

ArticleJournal of cachexia, sarcopenia and muscle2025

Loss of popdc3 Impairs Mitochondrial Function and Causes Skeletal Muscle Atrophy and Reduced Swimming Ability in Zebrafish.

Chen-Chen Sun, Zhang-Lin Chen, Dong Yang, Jiang-Ling Xiao, Xiang-Tao Chen, Xi-Yang Peng, Xiu-Shan Wu, Chang-Fa Tang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

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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

1 citing paper in PubMed.

  1. 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

8 authors.

Chen-Chen SunKey Laboratory of Physical Fitness and Exercise Rehabilitation, College of Physical Education, Hunan Normal University, Changsha, Hunan, China.ORCID 0000-0001-5784-3365
Zhang-Lin ChenKey Laboratory of Physical Fitness and Exercise Rehabilitation, College of Physical Education, Hunan Normal University, Changsha, Hunan, China.
Dong YangKey Laboratory of Physical Fitness and Exercise Rehabilitation, College of Physical Education, Hunan Normal University, Changsha, Hunan, China.
Jiang-Ling XiaoKey Laboratory of Physical Fitness and Exercise Rehabilitation, College of Physical Education, Hunan Normal University, Changsha, Hunan, China.
Xiang-Tao ChenKey Laboratory of Physical Fitness and Exercise Rehabilitation, College of Physical Education, Hunan Normal University, Changsha, Hunan, China.
Xi-Yang PengKey Laboratory of Physical Fitness and Exercise Rehabilitation, College of Physical Education, Hunan Normal University, Changsha, Hunan, China.
Xiu-Shan WuCenter for Heart Development, College of Life Sciences, Hunan Normal University, Changsha, China.
Chang-Fa TangKey Laboratory of Physical Fitness and Exercise Rehabilitation, College of Physical Education, Hunan Normal University, Changsha, Hunan, China.

Funding

Hunan Provincial Natural Science Foundation of China 2024JJ6177National Natural Science Foundation of China 81801392National Students' Platform for Innovation and Entrepreneurship Training Program S202310542035Postgraduate Scientific Research Innovation Project of Hunan Province CX20230492Research Foundation of Hunan Province Education Department 23B0840
6 · The paper itself

Abstract

backgroundThe Popeye domain containing 3 (POPDC3) protein is essential for the maintenance of skeletal muscle homeostasis. POPDC3 is a pathogenic variant gene of limb-girdle muscular dystrophy (LGMD), and its variants lead to LGMDR26. At the animal level, zebrafish larvae with popdc3 mutations develop tail curls and muscle atrophy. However, the mechanism of skeletal muscle atrophy induced by POPDC3 variants/loss remains unclear.

methodsEight-month-old male WT and popdc3 mKO zebrafish were used for this research. Loli Track (Denwmark) and Loligo Swimming Respirometer were used to observe the zebrafish's swimming ability. The zebrafish skeletal muscle structure and cross-sectional area (CSA) were observed and counted by transmission electron microscopy (TEM), H&E and wheat germ agglutinin (WGA). Enriched genes and signalling pathways were analysed using RNA sequencing, and the effects of popdc3 mKO on zebrafish skeletal muscle mitochondrial respiration, biogenesis and dynamics were examined to investigate possible mechanisms.

resultsThe swimming ability of popdc3 mKO zebrafish was reduced, and as evidenced by the reluctance to move, fewer movement trajectories, the total distance travelled (p < 0.001), the average velocity of movement (p < 0.001), oxygen consumption (MO

conclusionsPOPDC3, a Popeye protein, plays an important role in controlling mitochondrial function and skeletal muscle mass and strength. Loss of popdc3 decreases mitochondrial respiration and mitochondrial biogenesis, disrupting kinetic homeostasis, which induces mitochondrial dysfunction and impaired protein turnover (reduced synthesis and increased degradation), leading to zebrafish skeletal muscle atrophy.

Indexed as

MitochondriaMuscle, SkeletalMuscular AtrophySwimmingZebrafish ProteinsAnimalsDisease Models, AnimalMaleZebrafishZebrafish Proteinsmitochondrial dysfunctionPOPDC3protein homeostasisskeletal muscle atrophyskeletal muscle mass

Identifiers

PMID40237439
PMCPMC12001256

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Registered trials

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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.