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Cancer-A Major Cardiac Comorbidity With Implications on Cardiovascular Metabolism. | LitMetric

AI Article Synopsis

  • - Cardiovascular diseases result from various risk factors, including high blood pressure, smoking, high cholesterol, and diabetes, which lead to conditions like vascular stenosis and coronary heart disease, but recent studies show that cancer and its treatments can also negatively affect cardiovascular health.
  • - Cancer induces metabolic changes in the body that can worsen heart health, with conditions like cachexia and sarcopenia leading to heart failure and higher mortality rates among cancer patients—highlighting the interconnectedness of the two diseases.
  • - The review highlights how specific molecular regulators and inflammatory markers link cardiovascular issues and cancer, and how certain cancer therapies can directly impact heart cells, underscoring the need to understand these interactions for better patient outcomes.

Article Abstract

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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8662519PMC
http://dx.doi.org/10.3389/fphys.2021.729713DOI Listing

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