Mechanisms of Aging in the Vasculature and Immune System in the Context of Hypertension
Researchers here review the evidence for chronic inflammation to contribute to the vascular dysfunction of hypertension, in which blood pressure increases to harmful levels. The particular focus is on the feedback loop in which inflammatory immune dysfunction contributes to dysfunction in the regulation of hematopoiesis, the manufacture of new immune cells by hematopoietic cells resident in bone marrow, which in turn causes greater inflammatory immune dysfunction. Sustained inflammatory signaling is harmful to tissue structure and function throughout the body, including the vasculature and systems that regulate blood pressure.
Hypertension is a highly prevalent chronic disease all around the world, and the pathogenic mechanism is complicated. The early and rapid decline of the function of human vascular system due to the aging of human body are characteristics of hypertension, which is accompanied by progressive pathological remodeling and arterial stiffening.
The pathogenetic action of oxidation and inflammation is the vital function in the process of endothelial dysfunction and arterial injury. Bone marrow is considered as the birthplace of the immune cell, and the role of bone marrow in hematopoiesis and immune response for the onset of hypertension has been confirmed. In turn, inflammatory and oxidative stress also affect the bone marrow and damage bone marrow function, causing a series of complications in hypertension, resulting in a vicious cycle. Recently, increasing evidence has suggested that bone marrow aging plays an important role in the onset and development of hypertension, and that the function of bone marrow in the pathogenesis of hypertension has been seriously overlooked. Bone marrow microvascular ageing is also involved in the progression of bone marrow ageing.
Thus, this review mainly focuses on bone marrow function in aging and hypertension progression, addresses the current studies on the roles of vascular aging, the bone marrow and the immune system in hypertension, and discusses their interaction and function in the pathogenesis of hypertension. Furthermore, some novel molecular pathological mechanisms are surveyed. This can add a new impetus to the mechanism research of hypertension onset.