Abstract
Vascular amyloidosis (VA) is a component of aging, but both VA and aging move forward together. Although, not all age-related molecules are involved with VA, some molecules are involved in a crosstalk between both of them. However, the cellular mechanism by which, vascular cells are phenotypically shifted to arterial remodeling, is not only involved in aging but also linked to VA. Additionally, patients with hypertension and atherosclerosis are susceptible to VA, while amyloidosis alone may provide fertile soil for the initiation and progression of subsequent hypertension and atherosclerosis. It is known that hypertension, atherosclerosis and amyloidosis can be viewed as accelerated aging. This review summarizes the available experimental and clinical evidence to help the reader to understand the advance and underlying mechanisms for VA involvement in and interaction with aging. Taken together, it is clear that VA, hypertension and atherosclerosis are closely intertwined with arterial aging as equal partners.
Highlights
Frontiers in GeneticsVascular amyloidosis (VA) is a component of aging, but both VA and aging move forward together
Amyloid is found in the aortic walls of almost 100% of the population above 50 years of age (Mucchiano et al, 1992), and aged people are susceptible to hypertension and atherosclerosis, which indicates that vascular amyloidosis (VA), hypertension and atherosclerosis are highly associated with aging
endothelial cells (ECs) Truran et al, 2014, Matrix Berghoff et al, 2003 EC Davies et al, 2015b, vascular smooth muscle cells (VSMCs) Hagggvist et al, 1999 (Agyare et al, 2014); If they deposit within the walls of the coronary artery, they will lead to angina pectoris, even ischemia cardiomyopathy; If they deposit within the wall of aorta, they will lead to hypertension, atherosclerosis, and even dissecting aneurysm eventually (Wang et al, 2010a)
Summary
Vascular amyloidosis (VA) is a component of aging, but both VA and aging move forward together. Not all age-related molecules are involved with VA, some molecules are involved in a crosstalk between both of them. The cellular mechanism by which, vascular cells are phenotypically shifted to arterial remodeling, is involved in aging and linked to VA. It is known that hypertension, atherosclerosis and amyloidosis can be viewed as accelerated aging. This review summarizes the available experimental and clinical evidence to help the reader to understand the advance and underlying mechanisms for VA involvement in and interaction with aging. It is clear that VA, hypertension and atherosclerosis are closely intertwined with arterial aging as equal partners
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