ACE I/D gene polymorphism is not a susceptibility factor to aortoiliac occlusive disease; however it may be an important factor in the development of AAA when coexisting with hypertension.
The results showed that ACE2 gene transfer significantly decreased the occurrence of AAAs and inhibited AAA formation in ApoE<sup>-/-</sup> mice by inhibiting the inflammatory response and MMP activation, and the mechanisms may involve decreased ERK and Ang II-nuclear factor kappa B signaling pathways.
Our findings define a critical role of APLN in AAA formation through induction of ACE2 and protection of vascular SMCs, whereas stable APLN analogs provide an effective therapy for vascular diseases.
Previous studies demonstrated that deficiency of angiotensin-converting enzyme 2 (ACE2) augmented angiotensin II (AngII)-induced atherosclerosis and abdominal aortic aneurysm (AAA) formation in hypercholesterolemic mice.
Radiologists can contribute value to patient care and reduce morbidity and mortality related to AAA by incorporating evidence-based management recommendations from the ACR and Society of Vascular Surgery into their report impression.
American College of Surgeons National Surgical Quality Improvement Program (ACS NSQIP) Participant Use File data (2005 to 2015) for patients undergoing pancreatectomy, hepatectomy, esophagectomy, abdominal aortic aneurysm repair, open aortoiliac repair, and lung resection were used for analysis.
Finally, the levels of Gsα and SM α-actin were significantly lower while those of HuR and KLF4 were higher in human AAA samples than adjacent nonaneurysmal aortic sections.
Conclusions The downregulated UBB, NFIA, and SPARCL1 might play key roles in both aortic occlusive disease and abdominal aortic aneurysm, while the upregulated ACTB might only involve in abdominal aortic aneurysm.
By confocal immunohistochemistry, both human and mouse AAA smooth muscle cells (smooth muscle α-actin positive) and macrophages (CD68 positive or Mac-2 positive) expressed aromatase.
Together, our data afford the new insight that miR-103a inhibited AAA growth via targeting ADAM10, which might be a promising therapeutic strategy to alleviate AAA.
Additionally, the rs12692386 mutated AG genotype of ADAM17 was significantly associated with increased ADAM17 expression (P=0.035) and TNF-α production (P=0.042) in AAA patients.