SGK1-Mediated Vascular Smooth Muscle Cell Phenotypic Transformation Promotes Thoracic Aortic Dissection Progression.

ABSTRACT:

Background

The occurrence of thoracic aortic dissection (TAD) is closely related to the transformation of vascular smooth muscle cells (VSMCs) from a contractile to a synthetic phenotype. The role of SGK1 (serum- and glucocorticoid-regulated kinase 1) in VSMC phenotypic transformation and TAD occurrence is unclear.

Methods

Four-week-old male Sgk1^F/F (Sgk1 floxed) and Sgk1^F/F;Tagln^Cre (smooth muscle cell-specific Sgk1 knockout) mice were administered β-aminopropionitrile monofumarate for 4 weeks to model TAD. The SGK1 inhibitor GSK650394 was administered daily via intraperitoneal injection to treat the mouse model of TAD. Immunopurification and mass spectrometry were used to identify proteins that interact with SGK1. Immunoprecip

SUBMITTER: Leng S 

PROVIDER: S-EPMC11748913 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature