SLC1A5 prevents aortic aneurysm and dissection by glutaminolytic-epigenetic orchestration of vascular smooth muscle cell homeostasis - PubMed
5 hours ago
- #Aortic Aneurysm
- #Vascular Smooth Muscle Cells
- #Glutamine Metabolism
- SLC1A5 is significantly downregulated in vascular smooth muscle cells (VSMCs) from patients and mice with aortic aneurysm and dissection (AAD).
- SLC1A5 deficiency exacerbates AAD formation, promoting VSMC phenotypic switch and inflammation.
- SLC1A5 preserves contractile phenotype by facilitating glutamine metabolite acetyl-CoA production and histone acetylation.
- SLC1A5 ameliorates inflammation by promoting acetylated STAT3 mitochondrial translocation, inhibiting its nuclear translocation.
- Enforced SLC1A5 expression in VSMCs alleviates experimental AAD, suggesting it as a therapeutic target.