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Review
. 2019 Apr 15;115(5):824-829.
doi: 10.1093/cvr/cvz058.

Inflammation: a common contributor to cancer, aging, and cardiovascular diseases-expanding the concept of cardio-oncology

Peter Libby  1 , Sebastian Kobold  2
Affiliations
Review

Inflammation: a common contributor to cancer, aging, and cardiovascular diseases-expanding the concept of cardio-oncology

Peter Libby et al. Cardiovasc Res. .

Abstract

Inflammation participates in the pathogenesis of both cancer and cardiovascular disease. This review examines the mechanistic commonalities between these two scourges of humanity through the lens of inflammation biology. Inflammatory pathways contribute to the initiation, the progression, and the complication of both malignant tumours and atherosclerotic plaques. Modulation of inflammatory pathways have proven transformative in the treatment of cancers and have crossed the threshold of clinical reality as treatments to reduce the risk of cardiovascular events. The finding that clonal haematopoiesis drives both leukaemia and cardiovascular events provides yet another link between these two seemingly disparate diseases. The nascent specialty of cardio-oncology has initially focused on the cardiovascular complications of cancer therapies. The recognition of a more profound pathophysiologic connection between cancer and cardiovascular diseases should expand the concept of cardio-oncology. Embracing the mechanistic connection and transcending traditional barriers between disciplines offers immense opportunities for speeding innovative research that can address the growing burden of both cancer and cardiovascular disease.

Keywords: Aging; Cancer; Cardio-oncology; Cardiovascular disease; Inflammation.

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Figures

Figure 1
Figure 1
Common mechanisms and mediators in cancer and in atherosclerosis. Cancer and atherosclerosis share many common pathological mechanisms as depicted. Numerous mediators implicated in these two seemingly diverse diseases operate in both. FGF, fibroblast growth factor; MMP, matrix metalloproteinase; PDGF, platelet-derived growth factor; TGF-β, transforming growth factor beta; VEGF, vascular endothelial growth factor.
Figure 2
Figure 2
Regulation of cell accumulation in cancer and in atherosclerosis. The accumulation of cells in both cancer and atherosclerosis depends on the balance of growth stimulators and growth suppressors. In addition, some mediators promote cell death including programme cell death by apoptosis, and other pathways oppose cell death. The text and Figure 1 mention some of the mediators involved in regulating this balance between proliferation, cytostasis, and cell death.
See this image and copyright information in PMC

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