ATAD3A Limits Aortic Dissection via Mito-Lysosome Contacts and Lipoylation - PubMed
2 hours ago
- #ATAD3A
- #Aortic Dissection
- #Cuproptosis
- ATAD3A overexpression reduces aortic dissection by decreasing mitochondria-lysosome contacts and limiting mitochondrial calcium influx.
- ATAD3A suppresses the FDXR/FDX1/LIAS lipoylation pathway, reducing DLST lipoylation and inhibiting cuproptosis in vascular smooth muscle cells.
- Pharmacological inhibitors of cuproptosis, such as tetrathiomolybdate and devimistat, attenuate aortic aneurysm and dissection severity in vivo.
- VSMC-specific ATAD3A knockdown accelerates vascular pathology, while systemic overexpression improves survival and reduces dilation in mouse models.
- Targeting the ATAD3A-DLST-cuproptosis axis provides therapeutic potential for aortic aneurysm and dissection.