Research Status of Traditional Chinese Medicine Intervention on TGF-<i>β</i>/Smads Pathway in the Treatment of Myocardial Fibrosis DOI

灵 张

Traditional Chinese Medicine, Journal Year: 2025, Volume and Issue: 14(03), P. 1178 - 1184

Published: Jan. 1, 2025

Language: Английский

Shaofu Zhuyu Decoction Inhibits Fibrosis in a Mouse Model of Endometriosis Through the Ampk/Tgf-Β1/Smads Pathway: Integrating Network Pharmacology and Experimental Validation in Vivo DOI
Bingbing Li, Meiqi Ding,

Xiangying Chen

et al.

Published: Jan. 1, 2025

Ethnopharmacological relevance: Shaofu Zhuyu decoction (SFZYD) is efficacious in treating endometriosis(EMs); however, the molecular mechanisms underlying its effect on endometriosis-related fibrosis remain unknown.Aim of study: To explore and interventional effects SFZYD.Materials methods: The Traditional Chinese Medicine Systems Pharmacology(TCMSP), China National Knowledge Infrastructure(CNKI), PubMed, DrugBank, DisGeNET databases were used to screen SFZYD targets, Gene Ontology(GO) Kyoto Encyclopedia Genes Genome(KEGG) enrichment analyses common targets performed using Database for Annotation, Visualization, Integrated Discovery platform key pathways. Mice divided into control, endometriosis model, low-dose SFZYD, high-dose Dinorgestrel groups. Ectopic lesion weights volumes evaluated post-intervention. Uterine or morphology assessed hematoxylin/eosin Masson's trichrome & Sirius red staining, respectively. expression 5′ adenosine monophosphate-activated protein kinase (AMPK), transforming growth factor β1 (TGF-β1), collagen type 1 alpha chain (COL1A1), smooth muscle actin (α-SMA), connective tissue (CTGF) detected qRT-PCR. Protein those factors, plus AMPK, p-AMPK, TGF-β1, Smad2/3, p-Smad2/3, COL1A1, α-SMA CTGF was immunohistochemistry western blotting.Results: Network pharmacology experiments suggested could modulate fibrosis-related pathways, including AMPK TGF-β Staining revealed excessive ectopic fibrosis, p-AMPK/AMPK downregulated model group, whereas α-SMA, upregulated. Low-dose most effectively reduced size inhibited by activating/phosphorylating inhibiting TGF-β1 Smad2/3 expression, downregulating expression.Conclusion: formation mice regulating AMPK/TGF-β1/Smads signaling prevent fibrosis.

Language: Английский

Citations

0

Ca2+ Signaling in Cardiac Fibroblasts: An Emerging Signaling Pathway Driving Fibrotic Remodeling in Cardiac Disorders DOI Creative Commons
Francesco Moccia, Antonio Totaro, Germano Guerra

et al.

Biomedicines, Journal Year: 2025, Volume and Issue: 13(3), P. 734 - 734

Published: March 17, 2025

Cardiac fibrosis is a scarring event that occurs in the myocardium response to multiple cardiovascular disorders, such as acute myocardial infarction (AMI), ischemic cardiomyopathy, dilated hypertensive heart disease, inflammatory diabetic and aortic stenosis. Fibrotic remodeling mainly sustained by differentiation of fibroblasts into myofibroblasts, which synthesize secrete most extracellular matrix (ECM) proteins. An increase intracellular Ca2+ concentration ([Ca2+]i) cardiac emerging critical mediator fibrogenic signaling cascade. Herein, we review mechanisms may shape signals involved fibroblast transdifferentiation myofibroblasts. We focus our attention on functional interplay between inositol-1,4,5-trisphosphate (InsP3) receptors (InsP3Rs) store-operated entry (SOCE). In accordance with this, InsP3Rs SOCE drive elicited Gq-protein coupled (GqPCRs) promote fibrotic remodeling. Then, describe additional sustain entry, including receptor-operated (ROCE), P2X receptors, Transient Receptor Potential (TRP) channels, Piezo1 channels. parallel, discuss pharmacological manipulation handling machinery promising approach mitigate or reverse disorders.

Language: Английский

Citations

0

Research Status of Traditional Chinese Medicine Intervention on TGF-<i>β</i>/Smads Pathway in the Treatment of Myocardial Fibrosis DOI

灵 张

Traditional Chinese Medicine, Journal Year: 2025, Volume and Issue: 14(03), P. 1178 - 1184

Published: Jan. 1, 2025

Language: Английский

Citations

0