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. 2021 Nov 26;12:729713. doi: 10.3389/fphys.2021.729713

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Copyright © 2021 Finke, Heckmann, Frey and Lehmann.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Scheme of interacting factors between heart failure (HF), coronary heart disease (CHD), cancer growth, and muscle atrophy. Cytokine release from the tumor (Ataxin-10, D2-HG, IL-1/6, TNF-α, and INF-γ) may influence cardiac function and muscle wasting. Released factors from the heart, such as Myostatin and SerpinA3 are able to regulate muscular and cancer growth. Alterations in microRNAs (miRs) and metabolic pathways, including the hexosamine biosynthesis pathways (HBPs), PGC-1α and Akt activation are regulating cardiac remodeling as well as tumor growth. The adaptations in metabolic signaling pathways may be influenced by chemotherapies, e.g., by VEGF inhibitors and doxorubicin. D2-HG, D-2-hydroxyglurate; INF-γ, Interferon-gamma; IL, Interleukin; PGC-1α, Peroxisome proliferator-activated receptor-gamma coactivator; Akt, Protein kinase B; TNF-α, Tumor necrosis factor alpha; VEGF, Vascular endothelial growth factor. Created with Biorender.com.