CCL2 and Hepatic fibrosis: Reported mechanisms of TLR4 signaling-induced HSC activation and liver fibrosis include (1) BMP and activin membrane-bound inhibitor BAMBI downregulation, a TGF-β signaling inhibitor in quiescent HSCs [22, 23]; (2) miR-29 downregulation, which targets COL I expression [24]; (3) increased levels of LPS and DAMPs directly activating TLR4 signaling thereby activating nuclear factor κB (NF-κB) and c-Jun N-terminal kinase (JNK) that induce the production of many pro-inflammatory chemokines like monocyte chemoattractant protein-1 (MCP-1) and CCL-5, which in turn promote HSC activation [25, 26].