Cellular and molecular mechanisms of intestinal fibrosis

Figure 1 Mechanisms of fibrogenesis. Inflammatory response to tissue damage promotes the release of fibrogenic molecules. These molecules increase activation and proliferation of ECM-producing cells. ECM: Extracellular matrix.

Figure 2 Transforming growth factor-α signaling and induction of gene transcription. Smad: Small mother against decapentaplegic; SARA: Smad anchor for receptor activation; TGF-β: Transforming growth factor β.

Figure 3 Components and effects of the renin-angiotensin system. ACE: Angiotensin-converting enzyme; AT1: Angiotensin II type 1 receptor; AT2: Angiotensin II type 2 receptor; AT4: Angiotensin II type 4 receptor; MAS: Mas receptor; RAS: Renin-angiotensin system.

Figure 4 Activation of the peroxisome proliferator activator receptor-γ pathway. Regulation of several genes involved in fibrogenesis. PPAR-γ: Peroxisome proliferator activator receptor-γ; PPRE: PPAR response elements; RXR: Retinoid X receptors; L: Ligand; FA: Fatty acids.

Figure 5 Features of mammalian target of rapamycin. mTORC1: Mammalian target of rapamycin complex1; mTORC2: Mammalian target of rapamycin complex 2; 4EBP1: 4E binding protein; S6K: S6 kinase; PKB/Akt: Protein kinase B; SGK: Serum- and glucocorticoid-inducible kinase; PKC: Protein kinase C.