Mechanisms underlying the cross‐talk between heart and cancer

Brancaccio, Mara; Pirozzi, Flora; Hirsch, Emilio; Ghigo, Alessandra

doi:10.1113/jp276746

Cited by 17 publications

(9 citation statements)

References 99 publications

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“…During cachexia, cardiac wasting can also occur, primarily as a consequence of cardiac proteins loss 2 . This is for example the case of cancer patients where cardiac wasting is often secondary to therapy with cardiotoxic anti-cancer drugs or the presence of the tumor that, by producing circulating mediators, promotes atrophy of cardiomyocytes and negatively impacts on cardiac contractility 4 . Vice versa, cardiac dysfunction itself promotes skeletal muscle wasting, a complication known as cardiac cachexia.…”

Section: Introductionmentioning

confidence: 99%

Understanding the common mechanisms of heart and skeletal muscle wasting in cancer cachexia

et al. 2021

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Cachexia is a severe complication of cancer that adversely affects the course of the disease, with currently no effective treatments. It is characterized by a progressive atrophy of skeletal muscle and adipose tissue, resulting in weight loss, a reduced quality of life, and a shortened life expectancy. Although the cachectic condition primarily affects the skeletal muscle, a tissue that accounts for ~40% of total body weight, cachexia is considered a multi-organ disease that involves different tissues and organs, among which the cardiac muscle stands out for its relevance. Patients with cancer often experience severe cardiac abnormalities and manifest symptoms that are indicative of chronic heart failure, including fatigue, shortness of breath, and impaired exercise tolerance. Furthermore, cardiovascular complications are among the major causes of death in cancer patients who experienced cachexia. The lack of effective treatments for cancer cachexia underscores the need to improve our understanding of the underlying mechanisms. Increasing evidence links the wasting of the cardiac and skeletal muscles to metabolic alterations, primarily increased energy expenditure, and to increased proteolysis, ensuing from activation of the major proteolytic machineries of the cell, including ubiquitin-dependent proteolysis and autophagy. This review aims at providing an overview of the key mechanisms of cancer cachexia, with a major focus on those that are shared by the skeletal and cardiac muscles.

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Section: Introductionmentioning

confidence: 99%

Understanding the common mechanisms of heart and skeletal muscle wasting in cancer cachexia

et al. 2021

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“…The concomitant onset of cardiac disease is critical because heart dysfunction hinders optimal management of cancer treatment, especially where aggressive therapies are employed. A vicious circle may therefore develop where cachexia induces HF and HF exacerbates global cachexia [12][13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

How progressive cancer endangers the heart: an intriguing and underestimated problem

Ausoni

Calamelli

Saccà

et al. 2020

Cancer Metastasis Rev

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Since it came into being as a discipline, cardio-oncology has focused on the prevention and treatment of cardiotoxicity induced by antitumor chemotherapy and radiotherapy. Over time, it has been proved that even more detrimental is the direct effect generated by cancer cells that release pro-cachectic factors in the bloodstream. Secreted molecules target different organs at a distance, including the heart. Inflammatory and neuronal modulators released by the tumor bulk, either as free molecules or through exosomes, contribute to the pathogenesis of cardiac disease. Progressive cancer causes cachexia and severe cardiac muscle wasting accompanied by cardiomyocyte atrophy, tissue fibrosis, and several functional impairments up to heart failure. The molecular mechanisms responsible for such a cardiac muscle wasting have been partially elucidated in animal models, but minimally investigated in humans, although severe cardiac dysfunction exacerbates global cachexia and hampers efficient anti-cancer treatments. This review provides an overview of cancer-induced structural cardiac and functional damage, drawing on both clinical and scientific research. We start by looking at the pathophysiological mechanisms and evolving epidemiology and go on to discuss prevention, diagnosis, and a multimodal policy of intervention aimed at providing overall prognosis and global care for patients. Despite much interest in the cardiotoxicity of cancer therapies, the direct tumor effect on the heart remains poorly explored. There is still a lack of diagnostic criteria for the identification of the early stages of cardiac disease in cancer patients, while the possibilities that there are for effective prevention are largely underestimated. Research on innovative therapies has claimed considerable advances in preclinical studies, but none of the molecular targets suitable for clinical application has been approved for therapy. These issues are critically discussed here.

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“…Cancer and HF are leading causes of death worldwide, and their incidence increases with the progressive aging of the population [1]. Although these two conditions have been considered as distinct entities for long time, recent evidence indicates that they are deeply connected [5]. Moreover, along with the amelioration of CVDs management, the incidence of cardiovascular death has significantly decreased over the past decades, and long-term survivors to cardiovascular events may develop other age-related diseases, such as cancer, with consequent increase in non-cardiological deaths [6•, 7•].…”

Section: Epidemiologymentioning

confidence: 99%

New-Onset Cancer in the HF Population: Epidemiology, Pathophysiology, and Clinical Management

Cuomo

Paudice

D’Angelo

et al. 2021

Curr Heart Fail Rep

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Purpose of Review Oncological treatments are known to induce cardiac toxicity, but the impact of new-onset cancer in patients with pre-existing HF remains unknown. This review focuses on the epidemiology, pathophysiological mechanisms, and clinical implications of HF patients who develop malignancies. Recent Findings Novel findings suggest that HF and cancer, beside common risk factors, are deeply linked by shared pathophysiological mechanisms. In particular, HF itself may enhance carcinogenesis by producing pro-inflammatory cytokines, and it has been suggested that neurohormonal activation, commonly associated with the failing heart, might play a pivotal role in promoting neoplastic transformation. Summary The risk of malignancies seems to be higher in HF patients compared to the general population, probably due to shared risk factors and common pathophysiological pathways. Additionally, management of these patients represents a challenge for clinicians, considering that the co-existence of these diseases significantly worsens patients’ prognosis and negatively affects therapeutic options for both diseases.

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Mechanisms underlying the cross‐talk between heart and cancer

Cited by 17 publications

References 99 publications

Understanding the common mechanisms of heart and skeletal muscle wasting in cancer cachexia

Understanding the common mechanisms of heart and skeletal muscle wasting in cancer cachexia

How progressive cancer endangers the heart: an intriguing and underestimated problem

New-Onset Cancer in the HF Population: Epidemiology, Pathophysiology, and Clinical Management

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