MyD88 in hepatic stellate cells enhances liver fibrosis via promoting macrophage M1 polarization.

ABSTRACT: During liver fibrosis, quiescent HSCs (qHSCs) are activated to become activated HSCs (aHSCs)/myofibroblasts. The signal adapter MyD88, an essential component of TLR signaling, plays an important role in liver fibrosis. However, far less is known about the specific effects of MyD88 signaling in both qHSCs and aHSCs in the progress of liver fibrosis. Here, we used a CCl₄-induced mouse fibrosis model in which MyD88 was selectively depleted in qHSCs (GFAP^MyD88-/- mice) or aHSCs (α-SMA^MyD88-/- mice). MyD88 deficiency in qHSCs or aHSCs attenuated liver fibrosis in mice and inhibited α-SMA-positive cell activation. Inhibition of MyD88 in HSCs decreased α-SMA and collagen I levels, inflammatory cell infiltration, and pro-inflammatory gene expression. Furthermore, M

SUBMITTER: Zhang J 

PROVIDER: S-EPMC9051099 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature