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Updated: Mar 2, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
Published on: June 3, 2018
EFFECT OF TRIPTOLIDE ON PROLIFERATION AND APOPTOSIS OF ANGIOTENSIN II-INDUCED CARDIAC FIBROBLASTS IN VITRO: A
Triptolide (TPL) inhibits cardiac fibroblast proliferation and promotes apoptosis by down-regulating the TGF-β1/Smad3 pathway. This suggests TPL as a potential therapeutic for myocardial fibrosis.
Area of Science:
- Cardiovascular Research
- Cell Biology
- Pharmacology
Background:
- Cardiac fibrosis is a significant contributor to heart disease.
- The role of triptolide (TPL) in cardiac fibroblast (CFb) function and fibrosis is largely unexplored.
- Angiotensin II (Ang II) is known to induce CFb proliferation.
Purpose of the Study:
- To investigate the effects of TPL on proliferation and apoptosis of Ang II-induced CFbs.
- To elucidate the underlying molecular mechanisms, specifically the TGF-β1/Smad3 signaling pathway.
Main Methods:
- CFbs were stimulated with Ang II to induce proliferation.
- TPL was administered at two dosages (10ng/ml and 100ng/ml).
- Cell viability (MTT assay), apoptosis (flow cytometry), hydroxyproline concentration, and TGF-β1/Smad3 mRNA expression (qRT-PCR) were assessed.
Main Results:
- Ang II significantly increased CFb proliferation.
- TPL treatment markedly reduced CFb viability and hydroxyproline concentration.
- TPL significantly promoted CFb apoptosis.
- TPL decreased the expression of TGF-β1 and Smad3 mRNA in Ang II-treated CFbs.
Conclusions:
- TPL inhibits rat cardiac fibroblast proliferation via down-regulation of the TGF-β1/Smad3 signaling pathway.
- TPL demonstrates potential as a therapeutic agent for myocardial fibrosis.
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