Genomics and Inflammation in Cardiovascular Disease

Chronic cardiovascular diseases are associated with inflammatory responses within the blood vessels and end organs. The origin of this inflammation has not been certain, and neither is its relationship to disease clear. There is a need to determine whether this association is causal or coincidental to the processes leading to cardiovascular disease. These processes are themselves complex: many cardiovascular diseases arise in conjunction with the presence of sustained elevation of blood pressure. Inflammatory processes have been linked to hypertension, and causality has been suggested. Evidence of causality poses the difficult challenge of linking the integrated and multifaceted biology of blood pressure regulation with vascular function and complex elements of immune system function. These include both, innate and adaptive immunity, as well as interactions between the host immune system and the omnipresent microorganisms that are encountered in the environment and that colonize and exist in commensal relationship with the host. Progress has been made in this task and has drawn on experimental approaches in animals, much of which have focused on hypertension occurring with prolonged infusion of angiotensin II. These laboratory studies are complemented by studies that seek to inform disease mechanism by examining the genomic basis of heritable disease susceptibility in human populations. In this realm too, evidence has emerged that implicates genetic variation affecting immunity in disease pathogenesis. In this article, we survey the genetic and genomic evidence linking high blood pressure and its end-organ injuries to immune system function and examine evidence that genomic factors can influence disease risk. © 2021 American Physiological Society. Compr Physiol 11:1-22, 2021.