SPOCK1 overexpression induced by platelet-derived growth factor-BB promotes hepatic stellate cell activation and liver fibrosis through the integrin α5β1/PI3K/Akt signaling pathway

Mechanisms and disease consequences of nonalcoholic fatty liver disease

“…The effects of STAT-1 and STAT-3 in this setting are dissociated, with STAT-1 driving T cell infiltration and fibrosis, whereas STAT-3 is linked to increased cancer development. Signaling by nuclear factor of activated T cells (NFATc4) similarly downregulates PPARa, preventing fatty acid oxidation, which leads to secretion of osteopontin 1, which, in turn, can activate stellate cells (Du et al, 2020;Song et al, 2020b).…”

EZH2‐mediated inhibition of KLF14 expression promotes HSCs activation and liver fibrosis by downregulating PPARγ

“…The R-HSCs cultured for 1 day were considered as quiescent HSCs, and the R-HSCs cultured for 10 days were deemed as activated HSCs. 24 Firstly, we measured the purity of R-HSCs by flow cytometry analyses, which showed the purity was 97.63% (Figure S1A). The quiescent HSCs had obvious blue-green autofluorescence under ultraviolet excitation, and they were positive for Desmin immunofluorescence staining (Figure S1B).…”

SPOCK1: New Mechanistic Insight into Liver Fibrosis

“…In the recent study, for the first time, we elucidated the roles, mechanisms, and implications of SPOCK1 in liver fibrosis [20]. We found that SPOCK1 expression was dramatically upregulated in human and rat fibrotic liver tissues and in activated primary rat HSCs.…”