ArticleMolecular biology reports2025
HSPA9/HMGB1 regulates myocardial fibrosis in atrial fibrillation via TGF-β1/Smad pathway and autophagy.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Hematopoietic cell-specific knockout Hspa9 impairs natural killer cell function and alters the Akt/mTOR axis in mice.Experimental and therapeutic medicine · 2026Article
- Proteomic signatures of mitochondrial dysfunction associated with atrial fibrillation in goats.Scientific reports · 2026Article
- MYC promotes myocardial fibrosis via METTL1-mediated m7G modification of HILPDA.Biology direct · 2026Article
- Microglia Mitochondrial Metabolism in Neurological Diseases.Molecular neurobiology · 2026Review
- The role of different types of programmed cell death in myocardial fibrosis: from mechanisms to therapeutics.Frontiers in cardiovascular medicine · 2026Review
- Elevated Serum HMGB1 Levels and Their Association with Stroke Risk of Paroxysmal Atrial Fibrillation.Journal of inflammation research · 2025Article
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Authors and funding
5 authors.
Funding
Abstract
backgroundAtrial fibrillation (AF) is a common arrhythmia often linked to myocardial fibrosis. This study investigates the molecular mechanisms underlying AF, focusing on HSPA9 as a key regulator of fibrosis and its interaction with the TGF-β1/Smad pathway.
methodsThe GSE79768 dataset was employed for differential gene expression analysis. Weighted Gene Co-expression Network Analysis (WGCNA) identified key modules associated with AF. Functional enrichment analyses and Protein-Protein Interaction (PPI) networks were performed. Mouse cardiac fibroblasts were subjected to Angiotensin II (Ang II), and gene, protein, and functional analyses were conducted using quantitative real-time polymerase chain reaction (qRT-PCR), Western blot (WB), immunofluorescence, Co-immunoprecipitation (Co-IP), Cell Counting Kit-8 (CCK-8), and cell migration assays. In vivo, Ang II-induced mice were detected with immunohistochemistry (IHC) and Hematoxylin and Eosin (H&E) staining for fibrosis.
resultsWGCNA identified a strong correlation with the brown module, highlighting HSPA9 as a key gene in AF. HSPA9 was upregulated in AF tissues and Ang II-treated fibroblasts. Knockdown of HSPA9 suppressed fibroblast proliferation, migration, and fibrosis marker expression. HSPA9 interacts with HMGB1 to stabilize it, activating the TGF-β1/Smad pathway. HMGB1 overexpression reversed the effects of HSPA9 knockdown. In vivo, HSPA9 knockdown alleviated myocardial fibrosis. HSPA9 inhibits autophagy via the TGF-β1/Smad pathway, making it a possible target for treatment for AF and fibrosis.
conclusionHSPA9 regulates myocardial fibrosis in AF by interacting with HMGB1 and activating the TGF-β1/Smad pathway. Targeting HSPA9 could be a promising therapeutic strategy for preventing or treating AF-associated myocardial fibrosis.
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