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Fig. 2 | Journal of Biomedical Science

Fig. 2

From: The novel role of ER protein TXNDC5 in the pathogenesis of organ fibrosis: mechanistic insights and therapeutic implications

Fig. 2

Summary of the molecular mechanisms by which TXNDC5 promotes organ fibrogenesis. Schematic illustration of the mechanisms by which TXNDC5 contributes to organ fibrosis. TGFβ-stimulated ER stress activates the ATF6 branch, which transcriptionally activates TXNDC5 by physically interacting with TXNDC5 promoter. Increased TXNDC5 levels promote fibrogenic responses through 4 context-dependent mechanisms including (1) facilitating proper folding of fibrogenic ECM proteins, (2) stabilizing TGFβ receptor 1, and activating TGFβ non-canonical (3) JNK and (4) STAT3 signaling

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