Evidence mapPaperPMID 42447741Full record

ArticleRedox biology2026

Inactivation of SERCA2 at Cys674 induces skeletal muscle atrophy by activating the TGFβ/Smad-S100a4 axis to promote inflammation.

Fei Nan, Siyao Liu, Shunyi Lei, Yu Peng, Hailong Zhang, Xun Chen, Shixin Jin, Yuanfu Mao, Dan Lin, Xiaoyong Tong and 1 more

Abstract read
In one paragraph

Article in Redox biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Fei NanThird Department of Orthopedics of the First Affiliated Hospital of Harbin Medical University, Harbin, China; Department of Rheumatology of the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Siyao LiuThird Department of Orthopedics of the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Shunyi LeiThird Department of Orthopedics of the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Yu PengSchool of Pharmaceutical Sciences, Chongqing University, Chongqing, China.
Hailong ZhangSchool of Pharmaceutical Sciences, Chongqing University, Chongqing, China.
Xun ChenSchool of Pharmaceutical Sciences, Chongqing University, Chongqing, China.
Shixin JinThird Department of Orthopedics of the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Yuanfu MaoThird Department of Orthopedics of the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Dan LinDepartment of Rheumatology of the First Affiliated Hospital of Harbin Medical University, Harbin, China.
Xiaoyong TongSchool of Pharmaceutical Sciences, Chongqing University, Chongqing, China. Electronic address: xiaoyongtong@cqu.edu.cn.
Yanlong QuThird Department of Orthopedics of the First Affiliated Hospital of Harbin Medical University, Harbin, China. Electronic address: quyanlong@hrbmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsDisuse-induced skeletal muscle atrophy is a major clinical challenge lacking effective targeted therapies. Sarco/endoplasmic reticulum Ca

methodsOxidized SERCA2 (C674-SO

resultsTotal SERCA2 protein levels were unchanged in atrophied muscles from patients and HLS mice, whereas C674-SO

conclusionsThe oxidative inactivation of the SERCA2 C674 site constitutes a novel mechanism driving skeletal muscle atrophy. The SERCA2-RAS-TGF-β/Smad-S100a4 signaling axis emerges as a highly promising therapeutic target for mitigating disuse-induced skeletal muscle wasting.

Indexed as

InflammationMuscle, SkeletalMuscular AtrophyS100 Calcium-Binding Protein A4Sarcoplasmic Reticulum Calcium-Transporting ATPasesSmad ProteinsTransforming Growth Factor betaAnimalsCell LineCysteineDisease Models, AnimalHumansMiceSignal TransductionAtp2a2 protein, mouseCysteineS100 Calcium-Binding Protein A4Sarcoplasmic Reticulum Calcium-Transporting ATPasesSmad ProteinsTransforming Growth Factor betaInflammationS100a4SERCA2Skeletal muscle atrophyTGFβ/Smad signaling pathway

Identifiers

PMID42447741
PMCPMC13382413

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.