Loss of CLOCK under high glucose upregulates ROCK1-mediated endothelial to mesenchymal transition and aggravates plaque vulnerability

Carotid atherosclerotic plaque is one of the main sources of ischemic stroke, and endothelial-to-mesenchymal transition (EndMT) is a major feature of atherosclerosis. Rho-associated coiled-coil-containing protein kinase 1 (ROCK1) activation, stimulated by high glucose, plays an important role in EndMT, and circadian locomotor output cycles protein kaput (Clock) deficiency leads to hyperglycemia and enhanced atherosclerosis in Clock Δ19/Δ19 apolipoprotein E (ApoE)−/− mice. These findings point to a mechanism whereby CLOCK exerts a protective effect against EndMT and atherosclerotic plaque accumulation.

Source: Atherosclerosis - May 24, 2018 Category: Cardiology Authors: Hanfei Tang, Mengjiao Zhu, Gefei Zhao, Weiguo Fu, Zhenyu Shi, Yong Ding, Xiao Tang, Daqiao Guo Source Type: research