FIGURE 6.

Potential mechanisms of action of antifibrotic therapies from organs other than the gut. Available therapies modulate growth factor and cytokine signaling, intracellular kinases, and extracellular matrix (ECM) remodeling. AKT, protein kinase B; ASK, apoptosis signal-regulating kinase; CASP, caspase; CTGF, connective tissue growth factor; EMT, epithelial-to-mesenchymal transition; ET, endothelin; ETR, endothelin receptor; FGF, fibroblast growth factor; FGFR, FGF receptor; HIMF, human intestinal myofibroblast; IL12, interleukin-12; IL12R, IL12 receptor; JAK, Janus kinase; JNK, c-Jun NH₂-terminal kinase; MKK, mitogen-activated protein kinase kinase; mTOR, mammalian target of rapamycin; PDGF, platelet-derived growth factor; PDGFR, PDGF receptor; PI3K, phosphoinositide 3-kinase; PPAR, peroxisome proliferator-activated receptor; Rho, Ras homolog family member; RIP, receptor-interacting serine/threonine protein; RXR, retinoid X receptor; STAT, signal transducer and activator of transcription protein; TAK, transforming growth factor-β activated kinase; TGF, transforming growth factor; TGFR, TGF receptor; Th, T helper cells; TNF, tumor necrosis factor; TNFR, TNF receptor; TRADD, TNFR1-associated signal transducer; TRAP, TNFR-associated factor; VEGF, vascular endothelial growth factor; VEGFR, VEGF receptor.