Cross-disease communication between cancer and heart failure provides a rational approach to prevention and treatment of both diseases

Abstract

Accumulating clinical data have demonstrated a clear positive association between cancer and cardiac disorders, particularly chronic heart failure (CHF). These two diseases can be mutual drivers of each other, and hence frequently co-occur in patients. The immune system is the core mechanism that eliminates transformed cells from our bodies. However, immune cells often play distinct or even conflicting roles in cancer and CHF. Moreover, CHF alters the properties of immune cells, particularly those of regulatory T cells. Our previous study showed that the oxidative phosphorylation capacity of peripheral blood mononuclear cells is impaired in CHF, leading to the increased production of reactive oxygen species. Therefore, the co-occurrence of cancer and CHF becomes a serious problem, affecting the treatment of both diseases, and consequently negatively affecting patient survival rates. To date, few methods have been identified that effectively treat both diseases at the same time. Mitochondria activity may change in immune cells during their activation and exhaustion, and in CHF. Mitochondria activity is also largely affected in myocardia in CHF. We here focus on the mitochondrial abnormalities of immune cells in cancer and CHF, and discuss possible ways to treat cancer and CHF at the same time by targeting mitochondrial abnormalities. Many cancer cells are inevitably produced daily in our bodies, mostly owing to enzymatic nucleotide errors of DNA replication and repair. Therefore, the possibility of ways to prevent cancer by preventing the onset of heart failure will also be discussed.

Keywords: PBMC; diet; disease prevention; exercise; immune-checkpoint inhibition; mitochondrial oxidative phosphorylation; myokine; reactive oxygen species.

Figure 1

Cancer and HF mutually promote each other. An unhealthy lifestyle contributes to the development of cancer and CHF, and they are mutual disease drivers. Anticancer drugs and regulatory T cells appear to have conflicting roles in cancer and HF. Mitochondrial function and reactive oxygen species (ROS) production in immune cells are potential therapeutic targets in both diseases.