炎症:动脉粥样硬化和糖尿病中血管钙化的罪魁祸首。
Inflammation: a culprit for vascular calcification in atherosclerosis and diabetes.
作者信息
Bessueille L, Magne D
机构信息
University of Lyon, ICBMS UMR CNRS 5246, Bâtiment Raulin, 43 Bd du 11 novembre 1918, 69622, Villeurbanne Cedex, France.
出版信息
Cell Mol Life Sci. 2015 Jul;72(13):2475-89. doi: 10.1007/s00018-015-1876-4. Epub 2015 Mar 8.
It is today acknowledged that aging is associated with a low-grade chronic inflammatory status, and that inflammation exacerbates age-related diseases such as osteoporosis, Alzheimer's disease, atherosclerosis and type 2 diabetes mellitus (T2DM). Vascular calcification is a complication that also occurs during aging, in particular in association with atherosclerosis and T2DM. Recent studies provided compelling evidence that vascular calcification is associated with inflammatory status and is enhanced by inflammatory cytokines. In the present review, we propose on one hand to highlight the most important and recent findings on the cellular and molecular mechanisms of vascular inflammation in atherosclerosis and T2DM. On the other hand, we will present the effects of inflammatory mediators on the trans-differentiation of vascular smooth muscle cell and on the deposition of crystals. Since vascular calcification significantly impacts morbidity and mortality in affected individuals, a better understanding of its induction and development will pave the way to develop new therapeutic strategies.
如今人们公认,衰老与低度慢性炎症状态相关,并且炎症会加剧与年龄相关的疾病,如骨质疏松症、阿尔茨海默病、动脉粥样硬化和2型糖尿病(T2DM)。血管钙化是衰老过程中也会出现的一种并发症,尤其与动脉粥样硬化和T2DM相关。最近的研究提供了令人信服的证据,表明血管钙化与炎症状态相关,并会因炎症细胞因子而加剧。在本综述中,一方面,我们建议突出关于动脉粥样硬化和T2DM中血管炎症的细胞和分子机制的最重要和最新发现。另一方面,我们将阐述炎症介质对血管平滑肌细胞转分化以及晶体沉积的影响。由于血管钙化会显著影响受影响个体的发病率和死亡率,更好地了解其诱导和发展将为开发新的治疗策略铺平道路。