Mitochondrial Dysfunction: A New Hallmark in Hereditable Thoracic Aortic Aneurysm Development

Cells, Journal Year: 2025, Volume and Issue: 14(8), P. 618 - 618

Published: April 21, 2025

Thoracic aortic aneurysms (TAAs) pose a significant health burden due to their asymptomatic progression, often culminating in life-threatening rupture, and the lack of effective pharmacological treatments. Risk factors include elevated hemodynamic stress on ascending aorta, frequently associated with hypertension hereditary genetic mutations. Among causes, Marfan syndrome is most prevalent, characterized as connective tissue disorder driven by FBN1 mutations that lead thoracic ruptures. Similarly, affecting TGF-β pathway underlie Loeys–Dietz syndrome, while genes encoding extracellular or contractile apparatus proteins, such ACTA2, are linked non-syndromic familial TAA. Despite differences origin, these conditions share central pathophysiological features, including medial degeneration, smooth muscle cell dysfunction, remodeling, which collectively weaken wall. Recent evidence highlights mitochondrial dysfunction crucial contributor aneurysm formation syndrome. Disruption matrix–mitochondrial homeostasis axis exacerbates wall further promoting development. Beyond its structural role maintaining vascular integrity, ECM plays pivotal supporting function. This intricate relationship between matrix integrity reveals novel dimension TAA pathophysiology, extending beyond established paradigms remodeling dysfunction. review summarizes potential unifying mechanism explores how understanding conjunction mechanisms pathogenesis, opens new avenues for developing targeted treatments address conditions. Mitochondrial boosters could represent clinical opportunity patients

Language: Английский

Targeted drug delivery systems for atherosclerosis

Journal of Nanobiotechnology, Journal Year: 2025, Volume and Issue: 23(1)

Published: April 23, 2025

Atherosclerosis is a complex cardiovascular disease driven by multiple factors, including aging, inflammation, oxidative stress, and plaque rupture. The progression of this often covert, emphasizing the need for early biomarkers effective intervention measures. In recent years, advancements in therapeutic strategies have highlighted potential targeting specific processes atherosclerosis, such as localization, macrophage activity, key enzymes. Based on this, review discusses role targeted drugs treatment atherosclerosis. It also focuses their clinical efficacy anti-atherosclerosis ability to provide more precise approaches. findings underscore that future research can concentrate exploring newer drug delivery systems further refine enhance long-term dynamic management

Language: Английский