Table 1 Selected biomarkers of mechanisms leading to excessive fibrosis

CCL2/MCP-1

Chemokines

Cenicriviroc [87, 88]

CCL2/MCP-1 leads to excessive fibrosis by promoting inflammatory responses, inducing fibroblast proliferation and differentiation, and mediating extracellular matrix remodeling [100]

TNF-\(\alpha \), IL-1, IL-6

Pro-inflammatory cytokines

Glucocorticoid

These pro-inflammatory cytokines can act synergistically to promote fibrosis by stimulating fibroblast activation, collagen production, and inflammation [101,102,103]

TGF-\(\beta \)

TGF-β superfamily

Pirfenidone [104, 105]

TGF-β leads to excessive fibrosis by activating fibroblasts, promoting extracellular matrix synthesis, regulating inflammatory response, and inhibiting apoptosis [92, 106]

VEGF-R, PDGF-R, FGF-R

Receptor Tyrosine Kinases

Nintedanib [107, 108]

Excessive activation of these receptors can lead to proliferation and differentiation of fibroblasts, as well as excessive synthesis and deposition of extracellular matrix proteins, leading to the development of fibrosis. In addition, the activation of these receptors can also cause the infiltration and activation of inflammatory cells, further aggravating the fibrotic process

FXR

Steroid/steroid hormone receptor superfamily

Obeticholic acid

FXR activation exerts anti-fibrotic effects by reducing inflammation, modulating TGF-β signaling [109, 110]

ROS

/

Machine perfusion [111]

ROS is involved in the occurrence and development of excessive fibrosis through mechanisms such as oxidative stress, inflammation, apoptosis and necrosis, oxidative protein modification, and fibrocyte activation [112]