Departments of Medicine and Ophthalmology, Boston University School of Medicine, MA 02118, USA.
J Dent Res. 2010 Feb;89(2):116-27. doi: 10.1177/0022034509355765. Epub 2009 Dec 30.
Hyperglycemia is the most prevalent characteristic of diabetes and plays a central role in mediating adverse effects on vascular cells during the progression of diabetic vascular complications. In diabetic microangiopathy, hyperglycemia induces biochemical and molecular changes in microvascular cells that ultimately progress to retinal, renal, and neural complications and extends to other complications, including advanced periodontal disease. In this review, we describe changes involving basement membrane thickening, tissue remodeling, gap junctions, inflammation, cytokines, and transcription factors, and their effects on the pathogenesis of diabetic microvascular complications. The majority of the changes described relate to retinal microangiopathy, since ultrastructural, structural, and biochemical alterations have been well-characterized in this tissue.
高血糖是糖尿病最常见的特征,在糖尿病血管并发症进展过程中,对血管细胞的不良影响起着核心作用。在糖尿病性微血管病中,高血糖会引起微血管细胞的生化和分子变化,最终导致视网膜、肾脏和神经并发症,并扩展到其他并发症,包括晚期牙周病。在这篇综述中,我们描述了涉及基底膜增厚、组织重塑、缝隙连接、炎症、细胞因子和转录因子的变化,以及它们对糖尿病性微血管并发症发病机制的影响。所描述的大多数变化都与视网膜微血管病变有关,因为在这种组织中已经很好地描述了超微结构、结构和生化改变。