Department of Law, Economics and Sociology, University "Magna Graecia" of Catanzaro, Catanzaro, Italy; Interuniversity Center of Phlebolymphology (CIFL), International Research and Educational Program in Clinical and Experimental Biotechnology, University "Magna Graecia" of Catanzaro, Catanzaro, Italy.
Department of Health Sciences, University "Magna Graecia" of Catanzaro, Catanzaro, Italy.
Ann Vasc Surg. 2023 Aug;94:378-389. doi: 10.1016/j.avsg.2023.04.008. Epub 2023 Apr 15.
This review aims to analyze biomolecular and cellular events responsible for arterial aneurysm formation with particular attention to vascular remodeling that determines the initiation and the progression of arterial aneurysm, till rupture.
This review was conducted searching libraries such as Web of Science, Scopus, ScienceDirect, and MEDLINE. Used keywords with various combinations were "arterial aneurysms," "biology," "genetics," "proteomics," "molecular," "pathophysiology," and extracellular matrix".
There are several genetic alterations responsible of syndromic and nonsyndromic disease that predispose to aneurysm formation. Extracellular matrix imbalance, mainly due to the alteration of vascular smooth muscle cells homeostasis, overexpression of metalloproteinases, and cytokines activation, determines weakness of the arterial wall that dilates thus causing aneurysmal disease. Altered mechanotransduction in the extracellular matrix may also trigger and sustain anomalous cellular and biochemical signaling. Different cell population such as vascular smooth muscle cells, macrophages, perivascular adipose tissue cells, and vascular wall resident stem cells are all involved at different levels.
Improving knowledge in vascular biology may help researchers and physicians in better targeting aneurysmal disease to better prevent and better treat such important disease.
本综述旨在分析导致动脉瘤形成的生物分子和细胞事件，特别关注决定动脉瘤发生和进展直至破裂的血管重构。
本综述通过检索 Web of Science、Scopus、ScienceDirect 和 MEDLINE 等数据库进行。使用了各种组合的关键词，如“动脉瘤”、“生物学”、“遗传学”、“蛋白质组学”、“分子”、“病理生理学”和“细胞外基质”。
有几种遗传改变导致了综合征和非综合征疾病，使动脉瘤形成的易感性增加。细胞外基质失衡，主要是由于血管平滑肌细胞稳态的改变、金属蛋白酶的过度表达和细胞因子的激活，导致动脉壁的脆弱性扩张，从而导致动脉瘤疾病。细胞外基质中改变的力学转导也可能引发和维持异常的细胞和生化信号。不同的细胞群体，如血管平滑肌细胞、巨噬细胞、血管周围脂肪组织细胞和血管壁固有干细胞，都在不同的水平上参与其中。
提高对血管生物学的认识，可能有助于研究人员和医生更好地针对动脉瘤疾病，以更好地预防和治疗这种重要的疾病。
