The mechanism of vascular remodeling in lung injury
Vascular remodeling during lung injury is an extremely complex biological process that involves cell proliferation,apoptosis,migration,and reorganization of the extracellular matrix(ECM).Vascular smooth muscle cells(VSMCs)and endothelial cells(ECs)play a vital role in the maintenance and repair of lung tissue structure.Through interactions and responses to various bioactive molecules like angiotensin Ⅱ(Ang Ⅱ),vascular endothelial growth factor(VEGF),and transforming growth factor-beta(TGF-β),they facilitate vascular remodeling.These molecules not only affect the proliferation and migration of VSMCs and ECs but also involve the fine regulation of vascular constriction,dilation,and activation of signaling pathways.These pathways include mitogen-activated protein kinase(MAPK),Rho A,and protein kinase C(PKC),which regulate cellular functions.Furthermore,the activation of calcium signaling pathways and increased generation of reactive oxygen species(ROS)due to cellular stress responses in hypoxic conditions are also essential factors in vascular remodeling.Understanding these complex interactions and the underlying molecular mechanisms is of great significance for developing therapeutic strategies for lung injury and related vascular disorders.This review aims to explore the roles of VSMCs and ECs in vascular remodeling,how bioactive molecules influence this process,and how these biological processes interact and are regulated,in order to provide new insights and strategies for future research and clinical treatment.
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