Cancer—A Major Cardiac Comorbidity With Implications on Cardiovascular Metabolism
Cardiovascular diseases have multifactorial causes. Classical cardiovascular risk factors, such as arterial hypertension, smoking, hyperlipidemia, and diabetes associate with the development of vascular stenoses and coronary heart disease. Further comorbidities and its impact on cardiovascular metab...
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Frontiers Media S.A.
2021
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oai:doaj.org-article:13b66569e7084ee48deb4f926a3c85482021-12-01T07:37:36ZCancer—A Major Cardiac Comorbidity With Implications on Cardiovascular Metabolism1664-042X10.3389/fphys.2021.729713https://doaj.org/article/13b66569e7084ee48deb4f926a3c85482021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fphys.2021.729713/fullhttps://doaj.org/toc/1664-042XCardiovascular diseases have multifactorial causes. Classical cardiovascular risk factors, such as arterial hypertension, smoking, hyperlipidemia, and diabetes associate with the development of vascular stenoses and coronary heart disease. Further comorbidities and its impact on cardiovascular metabolism have gotten more attention recently. Thus, also cancer biology may affect the heart, apart from cardiotoxic side effects of chemotherapies. Cancer is a systemic disease which primarily leads to metabolic alterations within the tumor. An emerging number of preclinical and clinical studies focuses on the interaction between cancer and a maladaptive crosstalk to the heart. Cachexia and sarcopenia can have dramatic consequences for many organ functions, including cardiac wasting and heart failure. These complications significantly increase mortality and morbidity of heart failure and cancer patients. There are concurrent metabolic changes in fatty acid oxidation (FAO) and glucose utilization in heart failure as well as in cancer, involving central molecular regulators, such as PGC-1α. Further, specific inflammatory cytokines (IL-1β, IL-6, TNF-α, INF-β), non-inflammatory cytokines (myostatin, SerpinA3, Ataxin-10) and circulating metabolites (D2-HG) may mediate a direct and maladaptive crosstalk of both diseases. Additionally, cancer therapies, such as anthracyclines and angiogenesis inhibitors target common metabolic mechanisms in cardiomyocytes and malignant cells. This review focuses on cardiovascular, cancerous, and cancer therapy-associated alterations on the systemic and cardiac metabolic state.Daniel FinkeDaniel FinkeDaniel FinkeMarkus B. HeckmannMarkus B. HeckmannMarkus B. HeckmannNorbert FreyNorbert FreyLorenz H. LehmannLorenz H. LehmannLorenz H. LehmannLorenz H. LehmannFrontiers Media S.A.articlecardio-oncologycancer metabolismcardiac metabolismcytokinessecond messengermetabolic shiftPhysiologyQP1-981ENFrontiers in Physiology, Vol 12 (2021) |
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cardio-oncology cancer metabolism cardiac metabolism cytokines second messenger metabolic shift Physiology QP1-981 |
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cardio-oncology cancer metabolism cardiac metabolism cytokines second messenger metabolic shift Physiology QP1-981 Daniel Finke Daniel Finke Daniel Finke Markus B. Heckmann Markus B. Heckmann Markus B. Heckmann Norbert Frey Norbert Frey Lorenz H. Lehmann Lorenz H. Lehmann Lorenz H. Lehmann Lorenz H. Lehmann Cancer—A Major Cardiac Comorbidity With Implications on Cardiovascular Metabolism |
description |
Cardiovascular diseases have multifactorial causes. Classical cardiovascular risk factors, such as arterial hypertension, smoking, hyperlipidemia, and diabetes associate with the development of vascular stenoses and coronary heart disease. Further comorbidities and its impact on cardiovascular metabolism have gotten more attention recently. Thus, also cancer biology may affect the heart, apart from cardiotoxic side effects of chemotherapies. Cancer is a systemic disease which primarily leads to metabolic alterations within the tumor. An emerging number of preclinical and clinical studies focuses on the interaction between cancer and a maladaptive crosstalk to the heart. Cachexia and sarcopenia can have dramatic consequences for many organ functions, including cardiac wasting and heart failure. These complications significantly increase mortality and morbidity of heart failure and cancer patients. There are concurrent metabolic changes in fatty acid oxidation (FAO) and glucose utilization in heart failure as well as in cancer, involving central molecular regulators, such as PGC-1α. Further, specific inflammatory cytokines (IL-1β, IL-6, TNF-α, INF-β), non-inflammatory cytokines (myostatin, SerpinA3, Ataxin-10) and circulating metabolites (D2-HG) may mediate a direct and maladaptive crosstalk of both diseases. Additionally, cancer therapies, such as anthracyclines and angiogenesis inhibitors target common metabolic mechanisms in cardiomyocytes and malignant cells. This review focuses on cardiovascular, cancerous, and cancer therapy-associated alterations on the systemic and cardiac metabolic state. |
format |
article |
author |
Daniel Finke Daniel Finke Daniel Finke Markus B. Heckmann Markus B. Heckmann Markus B. Heckmann Norbert Frey Norbert Frey Lorenz H. Lehmann Lorenz H. Lehmann Lorenz H. Lehmann Lorenz H. Lehmann |
author_facet |
Daniel Finke Daniel Finke Daniel Finke Markus B. Heckmann Markus B. Heckmann Markus B. Heckmann Norbert Frey Norbert Frey Lorenz H. Lehmann Lorenz H. Lehmann Lorenz H. Lehmann Lorenz H. Lehmann |
author_sort |
Daniel Finke |
title |
Cancer—A Major Cardiac Comorbidity With Implications on Cardiovascular Metabolism |
title_short |
Cancer—A Major Cardiac Comorbidity With Implications on Cardiovascular Metabolism |
title_full |
Cancer—A Major Cardiac Comorbidity With Implications on Cardiovascular Metabolism |
title_fullStr |
Cancer—A Major Cardiac Comorbidity With Implications on Cardiovascular Metabolism |
title_full_unstemmed |
Cancer—A Major Cardiac Comorbidity With Implications on Cardiovascular Metabolism |
title_sort |
cancer—a major cardiac comorbidity with implications on cardiovascular metabolism |
publisher |
Frontiers Media S.A. |
publishDate |
2021 |
url |
https://doaj.org/article/13b66569e7084ee48deb4f926a3c8548 |
work_keys_str_mv |
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