Roles of Autophagy, Mitophagy, and Mitochondria in Left Ventricular Remodeling after Myocardial Infarction

Figures

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  Fig. 1.. After myocardial infarction, the cardiac injury repair process is a complex multi-stage pathophysiological process involving inflammation, neovascularization, and myocardial regeneration. Nppa, natriuretic peptide A; SUMO1, small ubiquitin-like modifier 1; VEGF, vascular endothelial growth factor; FABP4, fatty acid binding protein 4; TGF-β, transforming growth factor beta; MCP-1, monocyte chemoattractant protein-1; Jund, JunD proto-oncogene; Nppb, natriuretic peptide B; Fos, Fos proto-oncogene; CUMOL, cumene; TGF, transforming growth factor; PDGF, platelet-derived growth factor.

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  Fig. 2.. The molecular mechanisms of cardiac remodeling involve various pathophysiological stimuli. VCAM-1, vascular cell adhesion molecule-1; ADM, adrenomedullin; CNP, C-type natriuretic peptide; BNP, B-type natriuretic peptide; GDF-15, growth differentiation factor 15; EVs, extracellular vesicles; PIIINP, procollagen III N-terminal propeptide; MMP-1, matrix metalloproteinase-1; TNF-α, tumor necrosis factor alpha; PICP, procollagen I C-terminal propeptide; CITP, chronic immune thrombocytopenia; sST2, soluble suppression of tumorigenicity 2; IL, interleukin; ncRNA, non-coding RNA; vW, von willebrand; NT-proBNP, N-terminal pro-brain natriuretic peptide; MR-proANP, midregional pro-attrial natriuretic peptide; TGF-β, transforming growth factor-β; ECM, extraCellular matrix.

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  Fig. 3.. Autophagy plays a role in myocardial remodeling in myocardial infarction. P-AKT, phosphorylated protein kinase B; P-mTOR, phosphorylated mammalian target of rapamycin.