Abstract

Abstract Vascular remodeling is a common pathological process in cardiovascular diseases and includes changes in cell proliferation, apoptosis and differentiation as well as vascular homeostasis. Mechanical stresses, such as shear stress and cyclic stretch, play an important role in vascular remodeling. Vascular cells can sense the mechanical factors through cell membrane proteins, cytoskeletons and nuclear envelope proteins to initiate mechanotransduction, which involves intercellular signaling, gene expression, and protein expression to result in functional regulations. Non-coding RNAs, including microRNAs and long non-coding RNAs, are involved in the regulation of vascular remodeling processes. Mechanotransduction triggers a cascade reaction process through a complicated signaling network in cells. High-throughput technologies in combination with functional studies targeting some key hubs and bridging nodes of the network can enable the prioritization of potential targets for subsequent investigations of clinical translation. Vascular mechanobiology, as a new frontier field of biomechanics, searches for principles of stress-growth in vasculature to elucidate how mechanical factors induce biological effects that lead to vascular remodeling, with the goal of understanding the mechanical basis of the pathological mechanism of cardiovascular diseases at the cellular and molecular levels. Vascular mechanobiology will play a unique role in solving the key scientific problems of human physiology and disease, as well as generating important theoretical and clinical results.

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