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Early growth response 1 exacerbates thoracic aortic aneurysm and dissection of mice by inducing the phenotypic switching of vascular smooth muscle cell through the activation of Krüppel‐like factor 5
Early growth response 1 may worsen chest aorta aneurysm and tearing in mice by causing blood vessel muscle cells to change through activating Krüppel-like factor 5
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Abstract
Egr1 expression increased in aortic tissues of mice with thoracic aortic aneurysm and dissection (TAAD).
- Egr1 is associated with the differentiation and phenotypic switching of vascular smooth muscle cells (VSMCs).
- Deficiency of SMC-specific Egr1 reduced TAAD severity and inhibited VSMC phenotypic switching.
- Knockdown of Egr1 led to decreased migration and proliferation of synthetic VSMCs.
- Overexpression of Krüppel-like factor 5 (KLF5) diminished the inhibitory effects of Egr1 deficiency on VSMCs.
- Egr1 may promote TAAD progression by enhancing KLF5's role in VSMC phenotypic switching.
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