Endothelial cell (EC)-specific Ctgf/Ccn2 expression increases EC reprogramming and atherosclerosis.

• Tác giả: Luke P Brewster, Xiangqin Cui, Rudy L Gleason, Carson Hoffmann, Kyung In Baek, Hanjoong Jo, Dong-Won Kang, Chanwoo Kim, Sandeep Kumar, Andrew Leask, Feifei Li, Jing Ma, Victor Omojola, Christian Park, Anastassia Pokutta-Paskaleva, Julia Raykin, Gloriani Sanchez Marrero, Roy Sutliff, Maiko Teichmann, Lucas Timmins, Hiromi Yanagisawa, Fujie Zhao
• Ngôn ngữ: eng
• Thông tin xuất bản: Netherlands : Matrix biology : journal of the International Society for Matrix Biology , 2025
• Bộ sưu tập: NCBI
• ID: 730441

Tóm tắt

Arterial endothelial cells (ECs) reside in a complex biomechanical environment. ECs sense and respond to wall shear stress. Low and oscillatory wall shear stress is characteristic of disturbed flow and commonly found at arterial bifurcations and around atherosclerotic plaques. Disturbed flow is pro-inflammatory to ECs. Arteries also stiffen with aging and/or the onset of vascular disease. ECs sense and respond to stiffening in a pro-fibrotic manner. Thus, flow and stiffening disturbances elicit EC responses that promote pathologic arterial remodeling. However, the pathways elicited by ECs under pathologic stiffening and disturbed flow are not well understood. The objective of this work was to discover and test the modifiability of key pathways in ECs. To do this we used the partial carotid ligation model to impose disturbed flow onto the precociously stiffened fibulin-5 knockout (Fbln5