Endoplasmic Reticulum Stress and Pathogenesis of Vascular Calcification

Frontiers in Cardiovascular Medicine

article

Zhenqi Rao¹  Yidan Zheng²  Li Xu¹  Zihao Wang¹  Ying Zhou¹  Ming Chen¹  Nianguo Dong¹  Zhejun Cai³  Fei Li¹ 

[1] Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology;Basic Medical School, Tongji Medical College, Huazhong University of Science and Technology;Department of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine

关键词: vascular calcification;    endoplasmic reticulum stress;    unfolded protein response;    chronic kidney disease;    atherosclerosis;    diabetes;   

DOI  :  10.3389/fcvm.2022.918056

学科分类：地球科学(综合)

来源: Frontiers

【 摘 要 】

Vascular calcification (VC) is characterized by calcium phosphate deposition in blood vessel walls and is associated with many diseases, as well as increased cardiovascular morbidity and mortality. However, the molecular mechanisms underlying of VC development and pathogenesis are not fully understood, thus impeding the design of molecular-targeted therapy for VC. Recently, several studies have shown that endoplasmic reticulum (ER) stress can exacerbate VC. The ER is an intracellular membranous organelle involved in the synthesis, folding, maturation, and post-translational modification of secretory and transmembrane proteins. ER stress (ERS) occurs when unfolded/misfolded proteins accumulate after a disturbance in the ER environment. Therefore, downregulation of pathological ERS may attenuate VC. This review summarizes the relationship between ERS and VC, focusing on how ERS regulates the development of VC by promoting osteogenic transformation, inflammation, autophagy, and apoptosis, with particular interest in the molecular mechanisms occurring in various vascular cells. We also discuss, the therapeutic effects of ERS inhibition on the progress of diseases associated with VC are detailed.

【 授权许可】

CC BY