Taghavi Yousof, Hassanshahi Gholamhossein, Kounis Nicholas G, Koniari Ioanna, Khorramdelazad Hossein
Geriatric Care Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Department of Ophthalmology and Otorhinolaryngology, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
J Cell Commun Signal. 2019 Dec;13(4):451-462. doi: 10.1007/s12079-018-00500-8. Epub 2019 Jan 3.
Diabetic retinopathy (DR) is considered as a diabetes-related complication that can render severe visual impairments and is also a risk factor for acquired blindness in both developed as well as developing countries. Through fibrovascular epiretinal membranes (ERMs), this condition can similarly lead to tractional retinal detachment. Laboratory efforts evaluating the DR pathogenesis can be provided by ocular vitreous fluid and ERMs resulting from vitrectomy. The clinical stages of DR are significantly associated with expression levels of certain chemokines, including monocyte chemotactic protein-1 (MCP-1) in the intraocular fluid. The MCP-1 is also a known potent chemotactic factor for monocytes and macrophages that can stimulate them to produce superoxide and other mediators. Following hyperglycemia, retinal pigmented epithelial (RPE) cells, endothelial cells, and Müller's glial cells are of utmost importance for MCP-1 production, and vitreous MCP-1 levels rise in patients with DR. Increased expression of the MCP-1 in the eyes can also play a significant role in the pathogenesis of DR. In this review, current clinical and laboratory progress achieved on the MCP-1 and the DR concerning neovascularization and inflammatory responses in vitreous and/or aqueous humor of DR patients was summarized. It was suggested that further exploration of the MCP-1/CCR2 axis association between clinical stages of DR and expression levels of inflammatory and angiogenic cytokines and chemokines, principally the MCP-1 might lead to potential therapies aiming at neutralizing antibodies and viral vectors.
糖尿病视网膜病变(DR)被认为是一种与糖尿病相关的并发症,可导致严重的视力损害,在发达国家和发展中国家都是后天失明的危险因素。通过纤维血管性视网膜前膜(ERM),这种情况同样可导致牵拉性视网膜脱离。评估DR发病机制的实验室研究可通过眼玻璃体液和玻璃体切除术后的ERM来进行。DR的临床阶段与某些趋化因子的表达水平显著相关,包括眼内液中的单核细胞趋化蛋白-1(MCP-1)。MCP-1也是一种已知的单核细胞和巨噬细胞强效趋化因子,可刺激它们产生超氧化物和其他介质。高血糖后,视网膜色素上皮(RPE)细胞、内皮细胞和Müller胶质细胞对于MCP-1的产生至关重要,DR患者的玻璃体MCP-1水平会升高。眼内MCP-1表达的增加在DR的发病机制中也可发挥重要作用。在本综述中,总结了目前在MCP-1以及DR方面在DR患者玻璃体和/或房水中新生血管形成和炎症反应方面取得的临床和实验室进展。有人提出,进一步探索DR临床阶段与炎症和血管生成细胞因子及趋化因子表达水平之间的MCP-1/CCR2轴关联,主要是MCP-1,可能会带来针对中和抗体和病毒载体的潜在治疗方法。