The best conservative option to avoid AAA rupture consists in smoking cessation and control of hypertension. Many biological factors influence rupture risk.
SummaryWound healing crucially relies on the mechanical activity of fibroblasts responding to TGFb1 and to forces transmitted across focal adhesions. Integrin-linked kinase (ILK) is a central adapter recruited to integrin b1 tails in focal adhesions mediating the communication between cells and extracellular matrix. Here, we show that fibroblast-restricted inactivation of ILK in mice leads to impaired healing due to a severe reduction in the number of myofibroblasts, whereas inflammatory infiltrate and vascularization of the granulation tissue are unaffected. Primary ILK-deficient fibroblasts exhibit severely reduced levels of extracellular TGFb1, a-smooth muscle actin (aSMA) production and myofibroblast conversion, which are rescued by exogenous TGFb1. They are further characterized by elevated RhoA and low Rac1 activities, resulting in abnormal shape and reduced directional migration. Interference with RhoA-ROCK signaling largely restores morphology, migration and TGFb1 levels. We conclude that, in fibroblasts, ILK is crucial for limiting RhoA activity, thus promoting TGFb1 production, which is essential for dermal repair following injury.
BackgroundThe most important structural proteins of the vascular wall are collagen and elastin. Genetically linked connective tissue diseases lead to degeneration, aneurysm formation and spontaneous dissection or rupture of arteries. The most well-known are Marfan syndrome, vascular Ehlers-Danlos syndrome (type IV), Loeys-Dietz syndrome and familial aortic aneurysms and dissections.ObjectiveThis review article addresses the current status of endovascular treatment options for important connective tissue diseases.Material and methodsEvaluation of currently available randomized studies and registry data.ResultsThe treatment of choice for patients that are mostly affected at a young age is primarily conservative or open repair. There is only limited evidence for endovascular aortic repair (EVAR) of abdominal aneurysms or thoracic endovascular aortic repair (TEVAR).ConclusionThe progression of the disease with dilatation leads to secondary endoleaks and high reintervention rates with uncertain long-term results. For this reason, there is currently consensus that EVAR and TEVAR should be limited to justified exceptional cases and emergency situations in patients with genetically linked aortic diseases.
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