PHB2 ameliorates ferroptosis and aortic aneurysm/dissection through NEDD4L-dependent ubiquitination of NCOA4 - PubMed
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- #Ubiquitination
- #Aortic Aneurysm
- #Ferroptosis
- PHB2 is significantly downregulated in aortic aneurysm/dissection (AAD) and plays a protective role.
- PHB2 overexpression mitigates ferroptosis, a form of iron-dependent cell death, in vascular smooth muscle cells (VSMCs).
- PHB2 promotes NCOA4 degradation via NEDD4L-mediated ubiquitination, limiting ferritinophagy and ferroptosis.
- Loss of PHB2 exacerbates AAD progression by increasing ferroptosis and aortic wall damage.
- The PHB2-NEDD4L-NCOA4 axis is identified as a novel regulatory pathway in AAD pathogenesis.