Aortic dissection and aortic aneurysms are currently among the most high-risk cardiovascular diseases due to their rapid onset and high mortality. Although aneurysm research has been extensive, the pathogenesis remains unknown. Studies have found that the TGF-β/Smad pathway and aneurysm formation appear linked. For example, the TGF-β signaling pathway was significantly activated in aneurysm development and aortic dissection. Aneurysms are not, however, mitigated following knockdown of TGF-β signaling pathway-related genes. Incidence and mortality rate of ruptured thoracic aneurysms increase with the down-regulation of the classical TGF-β signaling pathway. In this review, we summarize recent findings and evaluate the differential role of classical and non-classical TGF-β pathways on aortic aneurysm. It is postulated that the TGF-β signaling pathway is necessary to maintain vascular function, but over-activation will promote aneurysms whereas over-inhibition will lead to bypass pathway over-activation and promote aneurysm occurrence.
Keywords: Aneurysm; Aortic dissection; Canonical TGF-β signaling; Non-canonical TGF-β signaling.
Copyright © 2019. Published by Elsevier B.V.