Evidence map›Paper›PMID 40183241›Full record

ArticleJournal of cachexia, sarcopenia and muscle2025

Nestin Regulates Autophagy-Dependent Ferroptosis Mediated Skeletal Muscle Atrophy by Ubiquitinating MAP 1LC3B.

Shunshun Han, Xiyu Zhao, Chunlin Yu, Can Cui, Yao Zhang, Qing Zhu, Mohan Qiu, Chaowu Yang, Huadong Yin

RetractedAbstract readRetracted Publication
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. It has been retracted, and should not be counted. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

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

6 citing papers in PubMed.

  1. Article
  2. Review
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  6. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Shunshun HanCollege of Animal Science and Technology, Key Laboratory of Livestock and Poultry Multi-Omics, Ministry of Agriculture and Rural Affairs, Sichuan Agricultural University, Chengdu, Sichuan, China.
Xiyu ZhaoCollege of Animal Science and Technology, Key Laboratory of Livestock and Poultry Multi-Omics, Ministry of Agriculture and Rural Affairs, Sichuan Agricultural University, Chengdu, Sichuan, China.
Chunlin YuAnimal Breeding and Genetics Key Laboratory of Sichuan Province, Sichuan Animal Science Academy, Chengdu, China.
Can CuiCollege of Animal Science and Technology, Key Laboratory of Livestock and Poultry Multi-Omics, Ministry of Agriculture and Rural Affairs, Sichuan Agricultural University, Chengdu, Sichuan, China.
Yao ZhangCollege of Animal Science and Technology, Key Laboratory of Livestock and Poultry Multi-Omics, Ministry of Agriculture and Rural Affairs, Sichuan Agricultural University, Chengdu, Sichuan, China.
Qing ZhuCollege of Animal Science and Technology, Key Laboratory of Livestock and Poultry Multi-Omics, Ministry of Agriculture and Rural Affairs, Sichuan Agricultural University, Chengdu, Sichuan, China.
Mohan QiuAnimal Breeding and Genetics Key Laboratory of Sichuan Province, Sichuan Animal Science Academy, Chengdu, China.
Chaowu YangAnimal Breeding and Genetics Key Laboratory of Sichuan Province, Sichuan Animal Science Academy, Chengdu, China.
Huadong YinCollege of Animal Science and Technology, Key Laboratory of Livestock and Poultry Multi-Omics, Ministry of Agriculture and Rural Affairs, Sichuan Agricultural University, Chengdu, Sichuan, China.ORCID 0000-0002-9546-5753

Funding

China Agriculture Research System of MOF and MARA CARS-40Sichuan Science and Technology Program 2021YFYZ0007Sichuan Science and Technology Program 2021YFYZ0031Sichuan Science and Technology Program 2023NSFSC1146
6 · The paper itself

Abstract

backgroundProgrammed cell death plays a critical role in skeletal muscle atrophy. Ferroptosis, an iron-dependent form of programmed cell death driven by lipid peroxidation, has been implicated in various diseases, but its role in skeletal muscle atrophy remains unclear.

methodsFerroptosis in skeletal muscle atrophy was investigated using two models: dexamethasone (Dex)-induced atrophy (n = 6 independent cell cultures per group) and simulated microgravity (n = 6 mice per group). Conditional Nestin knockout (KO) mice were generated using CRISPR/Cas9 (n = 6-8 mice per group), with wild-type (WT) controls (n = 6-8). Phenotypic analyses included histopathology (HE staining), functional assessments (muscle strength, weight analysis, treadmill), and dystrophy evaluation (dystrophin staining). Molecular analyses involved flow cytometry, ELISA, transmission electron microscopy, PI staining, and IP/MS to delineate Nestin-regulated ferroptosis pathways in skeletal muscle atrophy.

resultsFerroptosis was significantly activated in both atrophy models, with a 2.5-fold increase in lipid peroxidation (p < 0.01), a 2-fold accumulation of Fe

conclusionsOur study identifies Nestin as a critical regulator of ferroptosis-autophagy crosstalk in skeletal muscle atrophy. Targeting Nestin-LC3B ubiquitination may offer novel therapeutic strategies for preventing muscle wasting in diseases such as cachexia and sarcopenia.

Indexed as

AutophagyFerroptosisMicrotubule-Associated ProteinsMuscle, SkeletalMuscular AtrophyNestinAnimalsDisease Models, AnimalMaleMiceMice, KnockoutMap1lc3b protein, mouseMicrotubule-Associated ProteinsNestinautophagyferroptosisMAP 1LC3Bnestinskeletal muscle atrophy

Identifiers

PMID40183241
PMCPMC11969254

What OpenQuestion holds

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LicenceCC BY
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.