title: Medical therapy of aortic aneurysms: a pathophysiology-based approach.
abstract: One of the critical points in the pathogenesis of aortic aneurysms (AAs) is the disruption of the balance between vascular extracellular matrix (ECM) deposition and degradation. AAs are common features in some genetically determined diseases of the connective tissue, such as Marfan and Ehlers-Danlos. Acquired factors determining an enhanced inflammatory state of the arterial wall also play a key role. Previous studies have determined the role of tumor growth factor β (TGF-β); as a principal mediator of the pathogenesis of the alterations of the arterial wall homeostasis in AAs. The medical management of any AA is mainly focused on the use of pharmacological agents that reduce hemodynamic stress of the aortic wall, since hypertension is the major risk factor for the enlargement and rupture of the AAs. However, this is far from being a comprehensive pathophysiology-based therapeutic approach. Drugs potentially able to reduce the release of TGF-β may play a role in the pathogenesis of the AAs. They work by improving matrix repair, decreasing the proteolytic pattern and inhibition of angiotensin-converting enzyme (ACE) as well as preventing angiotensin II-induced angiotensin type-1 receptor (AT1R) activation. A new pathophysiology-based therapeutic approach, involving the mechanisms leading to the rupture of the AAs, could represent an additional tool in combination with the current established antihypertensive therapy.
authors.affiliation: Department of Medicine, Division of Diabetes, University of Texas Health Science Center at San Antonio, USA.
authors.forename: Giovanna
authors.initials: G
authors.lastname: Muscogiuri
authors.forename: Gian Pio
authors.initials: GP
authors.lastname: Sorice
authors.forename: Devjit
authors.initials: D
authors.lastname: Tripathy
authors.forename: Alberto O
authors.initials: AO
authors.lastname: Chavez
authors.forename: Alberto
authors.initials: A
authors.lastname: Davalli
authors.forename: Richard A
authors.initials: RA
authors.lastname: Lange
authors.forename: Franco
authors.initials: F
authors.lastname: Folli
mesh_terms: D000818:Animals; D001014:Aortic Aneurysm / Q000188:drug therapy* / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D050197:Atherosclerosis / Q000150:complications; D015551:Autoimmunity; D020022:Genetic Predisposition to Disease; D006801:Humans; D006973:Hypertension / Q000150:complications; D007333:Insulin Resistance; D045726:Metalloproteases / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D012307:Risk Factors; D016212:Transforming Growth Factor beta / Q000037:antagonists & inhibitors / Q000235:genetics
chemical_list: D016212:Transforming Growth Factor beta; D045726:Metalloproteases