Changes in tumor and cardiac metabolism upon immune checkpoint

Figures

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  Fig. 1. Mechanisms of immune-checkpoint inhibition. Binding of PD-1, LAG-3, and CTLA-4 inhibits T-cell activation and immune response (A). Immune-checkpoint inhibition by anti-PD1, anti-LAG-3, and anti-CLTA-4 allows T-cell activation (B). This results in changes in T-cell metabolism and gene transcription, as well as anti-tumor response and potentially cardiovascular immune-related adverse events (C). Figure created with Biorender.com

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  Fig. 2. Metabolic pathways in cardiomyocytes and alterations caused by cancer. In healthy myocardium, energy-yielding substrates are converted to Acetyl-CoA, which subsequently enters the TCA cycle. The red boxes indicate alterations in cardiac metabolism under pathological conditions. In diseased cardiomyocytes, glucose becomes the primary energy source. Mutations in IDH1 and IDH2 disrupt ATP production in diseases like acute myeloid leukemia (AML), suggesting that they could also contribute to cardiomyopathy. Additionally, biallelic loss-of-function variants in genes encoding succinate dehydrogenase (SDH) subunits lead to succinate accumulation, which is associated with dilated cardiomyopathy (DCM), cardiovascular disease (CVD), and ischemia–reperfusion injury. 2-HGA 2-Hydroxyglutarate, CVD Cardiovascular Disease, CoA Coenzyme A, DCM Dilated Cardiomyopathy, IDH Isocitrate Dehydrogenase, mCPT1 Muscle Form of Carnitine Palmitoyl Transferase, PDH Pyruvate Dehydrogenase, SDH Succinate Dehydrogenase, α-KDHG α-Ketoglutarate Dehydrogenase. Figure created with Biorender.com