Metabolic reprogramming in cardiac fibrosis: mechanisms, crosstalk, and therapeutic interventions

Figures

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  Figure 1. Crosstalk of metabolic reprogramming in cardiac fibrosis. Overview of crosstalk of metabolic reprogramming including glucose metabolism, lipid metabolism, and amino acid metabolism, as well as their crosstalk through shared intermediates (such as acetyl-CoA and α-KG) and epigenetic regulation in cardiac fibrosis.↑, increase/activation; ↓, decrease/inhibition. Ac, acetylation; Ser, serine; Gly, glycine; OAA, oxaloacetate. Created with BioGDP.com.

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  Figure 2. Schematic diagram of cardiac metabolic reprogramming in heart failure. Blue arrows indicate downregulation; red arrows indicate upregulation. During the progression of heart failure, fatty acid β−oxidation and glucose oxidation show a decreasing trend, while ketone body oxidation is compensatorily increased. MCT, monocarboxylate transporter; CD36/FAT, fatty acid translocase; PDH, pyruvate dehydrogenase; SCOT, succinyl−CoA:3−ketoacid CoA transferase. Created with BioGDP.com.

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  Figure 3. Therapeutic targeting of metabolic crosstalk in cardiac fibrosis. Anti-fibrotic interventions grouped by metabolic pathway. The signaling intersection indicates the anticipated therapeutic effects on key pathways, highlighting the crosstalk between metabolic pathways. Emerging strategies include gene therapy and natural products/nutritional interventions. ↑, increase/activation; ↓, decrease/inhibition. Created with BioGDP.com.