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. 2020 Jun 29;10(18):7993–8017. doi: 10.7150/thno.47826

Figure 5.

Figure 5

Molecular links between autophagy and cardiac fibrosis. Mounting evidence shows that autophagy plays contradictory roles in cardiac fibrosis. (A) The overexpression of several miRNAs, including miR-26a-5p and miR-221, or the downregulation of miR-200b suppress the activation of cardiac fibroblasts and autophagy flux. Furthermore, the activation of autophagy promotes cardiac fibrosis by regulating PARP-1, TGF-β/Smad and PKCβ1/ERK1/2 signaling pathways. (B) Accumulating evidence suggests that the activation of autophagy improves cardiac fibrosis illustrated by a variety of studies using specific-gene KO (CTSB, p8, Atg7 and SIRT7) mouse models. Panel B represents how autophagy-related signaling pathways, including SPRED2, PPAR, HMGB1, JNK/c-JUN, HSP27 and TAX1BP1/NF-κB pathways, and unfolded protein reactions contribute to cardiac fibrosis. CHMP2B: charged multivesicular body protein 2B; Ddit4: damage inducible transcript 4; DNMT3A: DNA methyltransferases 3A; HMGB1: high-mobility group box-1; PDLIM1: PDZ and LIM domain 1; SPRED2: sprouty-related protein with an EVH domain 2.