Deficiency in Aim2 affects viability and calcification of vascular smooth muscle cells from murine aortas and angiotensin-II induced aortic aneurysms.
Markus WortmannMuhammad ArshadMaani HakimiDittmar BöcklerSusanne DihlmannPublished in: Molecular medicine (Cambridge, Mass.) (2020)
Our results suggest a role for Aim2 in regulating VSMC proliferation and transition to an osteoblast-like or osteoclast-like phenotype, thereby modulating the response of VSMC in aortic remodeling and AA formation.
Keyphrases
- angiotensin ii
- smooth muscle
- aortic valve
- angiotensin converting enzyme
- vascular smooth muscle cells
- signaling pathway
- left ventricular
- pulmonary artery
- aortic dissection
- high glucose
- diabetic rats
- chronic kidney disease
- heart failure
- drug induced
- bone loss
- replacement therapy
- oxidative stress
- pulmonary hypertension
- pulmonary arterial hypertension
- endothelial cells