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Article

Smad3 gene C-terminal phosphorylation site mutation exacerbates CCl4-induced hepatic fibrogenesis by promoting pSmad2L/C-mediated signaling transduction.

Naunyn-Schmiedeberg's archives of pharmacology - 1 Aug 2021

Yang Juan, Gong Yongfang, Xu Wenjing, Li Lili, Shi Zhenghao, Wang Qin, He Yinghao, Zhang Chong, Luo Chenchen, Fang Zhirui, Yang Yan

Abstract excerpt

Current researches have confirmed that Smads, mediators of TGF-β signaling, are strictly controlled by domain-specific site phosphorylation in the process of hepatic disease. Usually, Smad3 phospho-isoform pSmad3L and pSmad3C are reversible and antagonistic; pSmad2L/C could act together with pSmad3L by stimulating PAI-1 expression and ECM synthesis to transmit fibrogenic signals. Our recent study found that...

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PMID: 34191114
DOI: 10.1007/s00210-021-02114-1

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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