Bone marrow inflammatory memory in cardiometabolic disease and inflammatory comorbidities

Cardiometabolic disorders are chief causes of morbidity and mortality, with chronic inflammation playing a crucial role in their pathogenesis. The release of differentiated myeloid cells with elevated pro-inflammatory potential, as a result of maladaptively trained myelopoiesis may be a crucial factor for the perpetuation of inflammation. Several cardiovascular risk factors, including sedentary lifestyle, unhealthy diet, hypercholesterolemia, and hyperglycemia, may modulate bone marrow hematopoietic progenitors, causing sustained functional changes that favour chronic metabolic and vascular inflammation. In the present review, we summarize recent studies that support the function of long-term inflammatory memory in progenitors of the bone marrow for the development and progression of cardiometabolic disease and related inflammatory comorbidities, including periodontitis and arthritis. We also discuss how maladaptive myelopoiesis associated with the presence of mutated hematopoietic clones, as present in clonal hematopoiesis, may accelerate atherosclerosis via increased inflammation.

Automated summary

Cardiometabolic disorders are major causes of illness and death, with chronic inflammation playing a crucial role in their development. The presence of maladaptively trained myeloid cells may contribute to the perpetuation of inflammation. Various cardiovascular risk factors can influence bone marrow hematopoietic progenitors, leading to sustained functional changes that promote chronic metabolic and vascular inflammation. This review summarizes recent studies supporting the role of long-term inflammatory memory in bone marrow progenitors for the development and progression of cardiometabolic disease and related inflammatory comorbidities.