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Figure 1. Cells involved in the onset of hepatic fibrosis. Liver fibrosis involves the interplay of several liver-resident and immune cell types. In response to liver injury from various causes, damaged hepatocytes trigger an inflammatory cascade, activating macrophages and promoting the release of ROS and pro-inflammatory cytokines, like TGF-β1. These signals stimulate the activation of quiescent HSCs into myofibroblasts. Activated HSCs proliferate in response to cytokines such as TGF-β and PDGF, producing type I collagen and extracellular matrix components, which drive fibrotic tissue deposition and scar formation. Created using BioRender. Chiabotto, G. (2025) https://BioRender.com/pbjeea3. AIH: Autoimmune hepatitis; ALD: alcohol-associated liver disease; CCLs: CC chemokine ligands; CXCL: CXC chemokine ligand; ECM: extracellular matrix; DAMPs: damage-associated molecular patterns; IFN-γ: interferon-γ; ILs: interleukins; LSEC: liver sinusoid endothelial cell; MAFLD: metabolic-associated fatty liver disease; MASH: metabolic dysfunction-associated steatohepatitis; MMPs: matrix metalloproteinases; NETs: neutrophil extracellular traps; NK: natural killer; NO: nitric oxide; PDGF: platelet-derived growth factor; ROS: reactive oxygen species; TGF-β: transforming growth factor-β; Th: T helper; TNF-α: tumor necrosis factor-α; Treg: T regulatory; VEGF: vascular endothelial growth factor; α-SMA: alpha-smooth muscle actin; TIMPs: tissue inhibitors of metalloproteinases; TLRs: Toll-like receptors; TGF-β1: transforming growth factor-β1; HSCs: hepatic stellate cells.