Description
Title: Marfan Syndrome: Thoracic Aortic Aneurysm Pathophysiology and Treatment Options
Abstract: About 20% of people with thoracic aortic disease have single-gene mutations that make the vessel more likely to develop aneurysms and/or acute aortic dissection, frequently without coexisting syndromic symptoms. Marfan syndrome (MFS), where mutations in the extracellular protein fibrillin-1 cause additional abnormalities in the heart, eyes, and skeleton, is one widely studied exception. The identification of key cellular and molecular determinants of thoracic aortic disease has been made possible by the use of MFS mouse models. Despite research efforts, the promise of turning experimental results from MFS mice into efficient drug therapies for MFS patients has not been realized. Here, we summarize a number of studies that suggest that the thoracic aortic disease seen in MFS mice is caused by endothelial dysfunction, improper angiotensin II, and TGF signaling. We also talk about how these studies have changed the way we think about potential new treatments that could halt the progression of aneurysms in this relatively common connective tissue disorder.
Keywords: angiotensin II; arterial disease; endothelial dysfunction; Marfan syndrome; NO signaling; oxidative stress; TGFβ; thoracic aortic aneurysm
Paper Quality: SCOPUS / Web of Science Level Research Paper
Subject: Biomolecules
Writer Experience: 20+ Years
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