Abstract
The exact molecular pathways underlying the multifactorial natural history of intracranial aneurysms (IAs) are still largely unknown, to the point that their understanding represents an imperative challenge in neurovascular research. Wall shear stress (WSS) promotes the genesis of IAs through an endothelial dysfunction causing an inflammatory cascade, vessel remodeling, phenotypic switching of the smooth muscle cells, and myointimal hyperplasia. Aneurysm growth is supported by endothelial oxidative stress and inflammatory mediators, whereas low and high WSS determine the rupture in sidewall and endwall IAs, respectively. Angioarchitecture, age older than 60 years, female gender, hypertension, cigarette smoking, alcohol abuse, and hypercholesterolemia also contribute to growth and rupture. The improvements of aneurysm wall imaging techniques and the implementation of target therapies targeted against inflammatory cascade may contribute to significantly modify the natural history of IAs. This narrative review strives to summarize the recent advances in the comprehension of the mechanisms underlying the genesis, growth, and rupture of IAs.
Highlights
Intracranial aneurysms (IAs) are life-threatening cerebrovascular pathologies with an incidence and prevalence of 1–6% and 3.2%, respectively, in the adult population [1].intracranial aneurysms (IAs) are focal enlargements of the arterial wall owing to the destruction of internal elastic lamina and tunica media
The IA wall enhancement allows the estimation of the inflammatory process at the arterial wall, which reflects the active progression of aneurysmal remodeling and demolition
The hemodynamic imbalance and focal variations of the Wall shear stress (WSS) were proven to be responsible for the genesis of IA
Summary
Intracranial aneurysms (IAs) are life-threatening cerebrovascular pathologies with an incidence and prevalence of 1–6% and 3.2%, respectively, in the adult population [1].IAs are focal enlargements of the arterial wall owing to the destruction of internal elastic lamina and tunica media. The occurrence of the IAs is related to genetic, hemodynamic, and inflammatory factors, which are responsible for the bulging of the arterial wall and, its rupture. We overview the most recent advances in the comprehension of the pathogenesis of IAs, focusing on the implications of gene mutations, inflammation pathways, and hemodynamic stress in the growth and rupture of the aneurysm.
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