Hematopoietic bone marrow renin-angiotensin system in health and disease

ABSTRACT

A locally active renin–angiotensin system (RAS) present in the bone marrow, which controls the growth, production, proliferation, and differentiation of hematopoietic cells. Local bone marrow RAS has also a role in neoplastic hematopoiesis such as genesis of leukemia and other malignancies. The local RAS in bone marrow plays important roles in atherosclerosis. The "bone marrow response-to-lipid” hypothesis integrates the knowledge that proatherogenic features of hematopoietic and nonhematopoietic progenitors are determined by the local actions of modified LDL on the expression of local RAS genes. There is a relationship between the autonomic nervous system and bone marrow cells. This association between bone marrow stromal cells, hematopoietic stem cell, and nerve terminals has been described as the "neuroreticular complex.” A characteristic feature of early hypertension is endothelial dysfunction. Bone marrow–related endothelial progenitor cells contribute in the healing of injured endothelium. Relationship between autonomous nervous system and bone marrow vasculature could be an important mechanism of the pathophysiology of hypertension. Local bone marrow RAS has important role in COVID-19 syndrome. ACE2 receptor is presented on the surface of hematopoietic stem/progenitor cells within the context of local bone marrow RAS that characterizes a target for the SARS-CoV-2 attack on bone marrow hematopoiesis. Bone marrow and lung tissue are in a harmony in hematopoiesis under the control of tissue RAS. RAS genes are critical at the initiation of the infections initiated by coronavirus family members and can have an important association with the exchange of immune genes in due clinical course following the infection. The aim of this chapter is to focus on the impacts of the local bone marrow RAS on definitive and neoplastic hematopoiesis, as well as its interrelationships among atherosclerosis, hypertension, and COVID-19 syndrome. © 2023 Elsevier Inc. All rights reserved.