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oai:repisalud.isciii.es:20.500.12105/154042024-09-27T08:51:33Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605

00925njm 22002777a 4500 dc Toral, Marta author de la Fuente-Alonso, Andrea author Campanero, Miguel R author Redondo, Juan Miguel author 2022-04 Recent studies have shown that NO is a central mediator in diseases associated with thoracic aortic aneurysm, such as Marfan syndrome. The progressive dilation of the aorta in thoracic aortic aneurysm ultimately leads to aortic dissection. Unfortunately, current medical treatments have neither halt aortic enlargement nor prevented rupture, leaving surgical repair as the only effective treatment. There is therefore a pressing need for effective therapies to delay or even avoid the need for surgical repair in thoracic aortic aneurysm patients. Here, we summarize the mechanisms through which NO signalling dysregulation causes thoracic aortic aneurysm, particularly in Marfan syndrome. We discuss recent advances based on the identification of new Marfan syndrome mediators related to pathway overactivation that represent potential disease biomarkers. Likewise, we propose iNOS, sGC and PRKG1, whose pharmacological inhibition reverses aortopathy in Marfan syndrome mice, as targets for therapeutic intervention in thoracic aortic aneurysm and are candidates for clinical trials. Br J Pharmacol. 2022 Apr;179(7):1287-1303 10.1111/bph.15694 1476-5381 British journal of pharmacology 34599830 http://hdl.handle.net/20.500.12105/15404 The NO signalling pathway in aortic aneurysm and dissection.