Journal
FRONTIERS IN CARDIOVASCULAR MEDICINE
Volume 7, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fcvm.2020.00064
Keywords
organ crosstalk; chronic inflammation; multimorbidity; metabolic syndrome; cardiorenal syndrome; heart failure; somatic mutation; clonal hematopoiesis of indeterminate potential (CHIP)
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Funding
- MEXT Japan [20H03679, 20H04956, 17K09589, 19H03648, 17KT0047, 20H04938, 18H05023]
- Japan Agency for Medical Research and Development, AMED [19gm5910021h9903, 19gm0610011h0406, 19gm5010002]
- Mitsui Life Social Welfare Foundation
- Cell Science Research Foundation
- Terumo life science Foundation
- Takeda Science Foundation
- Naito Foundation
- Uehara Memorial Foundation
- Ono Medical Research Foundation
- SENSHIN Medical Research Foundation
- Tokyo Biochemical Research Foundation
- Suzuken Memorial Foundation
- Novartis Foundation for the Promotion of Science
- Grants-in-Aid for Scientific Research [18H05023, 17KT0047, 17K09589, 20H04938, 20H03679, 20H04956, 19H03648] Funding Source: KAKEN
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The close association among cardiovascular, metabolic, and kidney diseases suggests a common pathological basis and significant interaction among these diseases. Metabolic syndrome and cardiorenal syndrome are two examples that exemplify the interlinked development of disease or dysfunction in two or more organs. Recent studies have been sorting out the mechanisms responsible for the crosstalk among the organs comprising the cardiovascular, metabolic, and renal systems, including heart-kidney and adipose-liver signaling, among many others. However, it is also becoming clear that this crosstalk is not limited to just pairs of organs, and in addition to organ-organ crosstalk, there are also organ-system and organ-body interactions. For instance, heart failure broadly impacts various organs and systems, including the kidney, liver, lung, and nervous system. Conversely, systemic dysregulation of metabolism, immunity, and nervous system activity greatly affects heart failure development and prognosis. This is particularly noteworthy, as more and more patients present with two or more coexisting chronic diseases or conditions (multimorbidity) due in part to the aging of society. Advances in treatment also contribute to the increase in multimorbidity, as exemplified by cardiovascular disease in cancer survivors. To understand the mechanisms underlying the increasing burden of multimorbidity, it is vital to elucidate the multilevel crosstalk and communication within the body at the levels of organ systems, tissues, and cells. In this article, we focus on chronic inflammation as a key common pathological basis of cardiovascular and metabolic diseases, and discuss emerging mechanisms that drive chronic inflammation in the context of multimorbidity.
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