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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Autores principales: Daniel Finke, Markus B. Heckmann, Norbert Frey, Lorenz H. Lehmann
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Publicado: Frontiers Media S.A. 2021
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spelling 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)
institution DOAJ
collection DOAJ
language EN
topic cardio-oncology
cancer metabolism
cardiac metabolism
cytokines
second messenger
metabolic shift
Physiology
QP1-981
spellingShingle 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
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