Endothelial activation and fibrotic changes are impeded by laminar flow-induced CHK1-SENP2 activity through mechanisms distinct from endothelial-to-mesenchymal cell transition
In this study, we have revealed a novel mechanism underlying the suppressive effects of L-flow on EC inflammation, migration, proliferation, apoptosis, and fibrotic changes through promoting CHK1-induced SENP2 S344 phosphorylation. The phospho-site mutation SENP2 S344A responds to L-flow through a distinct mechanism, which involves the upregulation of both mesenchymal and EC marker genes.PMID:37711550 | PMC:PMC10499395 | DOI:10.3389/fcvm.2023.1187490
Source: Atherosclerosis - Category: Cardiology Authors: Minh T H Nguyen Masaki Imanishi Shengyu Li Khanh Chau Priyanka Banerjee Loka Reddy Velatooru Kyung Ae Ko Venkata S K Samanthapudi Young J Gi Ling-Ling Lee Rei J Abe Elena McBeath Anita Deswal Steven H Lin Nicolas L Palaskas Robert Dantzer Keigi Fujiwara M Source Type: research
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