Novel signaling axis of FHOD1-RNF213-Col1 α/Col3α in the pathogenesis of hypertension-induced tunica media thickening

Hypertension-induced tunica media thickening (TMT) is the most important fundamental for the subsequent complications like stroke and cardiovascular diseases. Pathogenically, TMT originates from both vascular smooth muscle cells (VSMCs) hypertrophy due to synthesizing more amount of intracellular contractile proteins and excess secretion of extracellular matrix. However, what key molecules are involved in the pathogenesis of TMT is unknown. We hypothesize that formin homology 2 domain-containing protein 1 (FHOD1), an amply expressed mediator for assembly of thin actin filament in VSMCs, is a key regulator for the pathogenesis of TMT.

Source: Journal of Molecular and Cellular Cardiology - July 21, 2023 Category: Cytology Authors: Yuanyuan Chen, Yuchan Yuan, Yuhan Chen, Xueze Jiang, Xuesheng Hua, Zhiyong Chen, Julie Wang, Hua Liu, Qing Zhou, Ying Yu, Zhenwei Yang, Yi Yu, Yongqin Wang, Qunshan Wang, Yigang Li, Jie Chen, Yuepeng Wang Source Type: research