Cardiomyocyte-derived HSPB1 regulates TGF-β1 maturation and inhibits endothelial-to-mesenchymal transition in myocardial fibrosis.

Jia Wang, Aoni Fu, Guoliang Tan, Haotian Yang, Jiang Zhou, Jianqiang Peng, Qinghai Zhang, Xiehong Liu

Abstract read

In one paragraph

Article in iScience, 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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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Jia WangHunan Provincial Key Laboratory of Emergency and Critical Care Metabonomics, Institute of Emergency Medicine, Hunan Provincial People's Hospital (The First Afliated Hospital of Hunan Normal University), Changsha, Hunan, China.

Aoni FuInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, Hengyang Medical School, University of South China, Hengyang, Hunan, China.

Guoliang TanDepartment of Cardiology, Hunan Provincial People's Hospital (The First Afliated Hospital of Hunan Normal University), Changsha, Hunan, China.

Haotian YangInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, Hengyang Medical School, University of South China, Hengyang, Hunan, China.

Jiang ZhouCollege of Clinical Laboratory, Changsha Medical University, Changsha, Hunan, China.

Jianqiang PengDepartment of Cardiology, Hunan Provincial People's Hospital (The First Afliated Hospital of Hunan Normal University), Changsha, Hunan, China.

Qinghai ZhangDepartment of Cardiology, Hunan Provincial People's Hospital (The First Afliated Hospital of Hunan Normal University), Changsha, Hunan, China.

Xiehong LiuHunan Provincial Key Laboratory of Emergency and Critical Care Metabonomics, Institute of Emergency Medicine, Hunan Provincial People's Hospital (The First Afliated Hospital of Hunan Normal University), Changsha, Hunan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial fibrosis after myocardial infarction is promoted by endothelial-to-mesenchymal transition (EndoMT) driven by TGF-β1. We investigated whether cardiomyocyte heat shock protein B1 (HSPB1) shapes this pathway. In mouse infarction models, cardiomyocyte-targeted HSPB1 overexpression reduced collagen deposition and preserved ventricular function, whereas HSPB1 knockdown exacerbated fibrosis and EndoMT activation. In endothelial assays, HSPB1 attenuated TGF-β1-induced Smad2/3 phosphorylation and mesenchymal marker expression. Mechanistically, HSPB1 modulated redox conditions to restrain disulfide-bond formation during pro-TGF-β1 maturation, reducing the secretion of mature TGF-β1. These results link cardiomyocyte redox homeostasis with paracrine control of endothelial plasticity and support HSPB1 as a therapeutic entry point to limit post-infarction fibrotic remodeling.

Indexed as

cardiovascular medicinemolecular biologymolecular biology experimental approach

Identifiers

PMID41816302

DOI10.1016/j.isci.2026.115028

PMCPMC12972742

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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.