Biotechnological Elucidation of Xinyin Tablet's Mechanism: SIRT1 Activation Attenuates Cardiac Fibrosis Via Suppressing Endothelial-to-Mesenchymal Transition.
Year: 2025
Type: article
Abstract: Background: , and other medicines, is clinically used to manage chronic heart failure (HF), yet its molecular mechanisms remain underexplored. Objectives: This study integrates biotechnological approaches to investigate how XYT mitigates cardiac fibrosis by targeting the SIRT1-mediated TGF-β/Smad signaling pathway. Materials and Methods: Transverse aortic constriction (TAC)-induced HF mice and TGF-β1-stimulated myocardial microvascular endothelial cells (MMECs) were employed. Echocardiography, histopathology, and molecular assays (qRT-PCR, Western blotting, siRNA transfection) were utilized to assess cardiac function, fibrosis, and signaling pathways. Results: XYT treatment significantly improved cardiac function (↑LVEF, LVFS; ↓LVIDs, LVIDd) and reduced collagen I/III deposition in TAC mice. Mechanistically, XYT upregulated SIRT1 expression while suppressing EndMT markers (↓α-SMA, ↑VE-cadherin) and TGF-β/Smad signaling (↓TGF-βR1, p-Smad2/3). Crucially, SIRT1 knockdown in MMECs abolished XYT's inhibitory effects on EndMT and TGF-β/Smad activation, confirming SIRT1's pivotal role. Conclusions: These findings highlight XYT's biotechnological relevance by linking SIRT1 activation to EndMT inhibition, offering a novel therapeutic strategy for cardiac fibrosis. This study underscores the potential of integrating traditional medicine with molecular biotechnology to develop targeted therapies for cardiovascular diseases.
Source: PubMed
Authors: Qiao Li, Taochun Ye, Qingmin Chu, Xin Shang, Min Liu
Language: English
Subfield: Cardiology and Cardiovascular Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W4413970854