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. 2026 Aug 24;17:1691999. doi: 10.3389/fphar.2026.1691999

FIGURE 3.

Diagram illustrating cellular mechanisms of hepatic fibrosis, showing apoptosis and cytokine storm with ROS, TNF-α, IL-1β, and IL-6; ECM deposition; activation of hepatic stellate cells (HSCs); and fibroblast-to-myofibroblast transformation, resulting in central fibrosis. The diagram also depicts key modulators of apoptosis (Bax/Bcl-2) and autophagy (Beclin-1/LC3). A color-coded key differentiates cell types and processes.

Central role of hepatic stellate cell (HSC) activation in liver fibrosis. Under normal conditions, HSCs remain quiescent. Upon liver injury or inflammatory stimulation, elevated levels of reactive oxygen species (ROS) and pro-inflammatory cytokines (e.g., TNF-α, IL-1β, and IL-6) induce HSC activation. Activated HSCs transdifferentiate into myofibroblasts, which overproduce the extracellular matrix (ECM), leading to fibrosis. Additionally, epithelial–mesenchymal transition (EMT) may further promote ECM deposition and fibrogenesis. In severe inflammation, a cytokine storm can exacerbate HSC activation and fibrosis progression. Arrows indicate regulatory or transformational relationships.