环状RNA参与调控糖尿病视网膜病变的研究进展

糖尿病视网膜病变(diabetic retinopathy,DR)是糖尿病在眼部的慢性微血管并发症之一,导致糖尿病患者视觉质量下降甚至失明事件发生率不断提高。然而目前为止,导致DR的病理改变机制十分复杂且未完全阐明,临床治疗多根据DR不同分期采取对症治疗,如视网膜激光光凝治疗、抗血管内皮因子治疗、玻璃体切割及剥膜手术等,仍缺乏安全有效的治疗方法,因此有必要寻找新的诊治靶标。随着分子生物学分析技术的发展,环状RNA(circular RNA,circRNA)成为目前重要的研究热点之一。据报道在多种因素的刺激下,基因的调节表达——circRNA通过调节视网膜微血管周细胞、视网膜微血管内皮细胞、视网膜色素上皮细胞等功能,参与到视网膜基底膜增厚、血管渗漏、细胞凋亡、炎症反应及新生血管增生等病理性过程来调控DR发生发展。故本文主要阐述环状RNA、竞争性内源性RNA以及微小RNA在DR病理改变分子机制、治疗前景中的研究进展,以期为临床及基础研究提供一定的参考。     

神经元退行性病变在糖尿病视网膜病变中的研究进展

糖尿病视网膜病变是糖尿病常见的并发症,作为微血管病变被广泛报道。研究发现视网膜神经元退行性病变在糖尿病视网膜病变早期已经发生,且在糖尿病视网膜病变进展过程中扮演重要角色。神经元退行性病变以神经元凋亡和胶质反应为主要特征,其发生机制包括高血糖、氧化应激、谷氨酸毒性、炎症等。糖尿病视网膜神经退行性病变与微血管病变的发生发展密切相关。     

糖尿病早期视网膜神经元退行性病变最新研究进展

糖尿病视网膜病变(diabetic retinopathy,DR)在早期被认为是一种微血管性疾病,多年来关于DR发病机制的研究主要集中在血管特征的改变上,包括血管渗透性的增加、新生血管的形成和黄斑水肿等.近年大量的视网膜电生理检查发现在糖尿病早期视网膜微血管发生损害前,视网膜神经元即发生一系列病理改变,提示DR是一种神经血管性疾病,这也可以解释DR患者很快发生的视功能减退.现将国内外关于糖尿病早期视网膜神经元退行性病变的最新研究进展作一综述,以期发现有效的视网膜神经元保护策略,从而减缓DR的进程.     

炎症在糖尿病视网膜病变中的作用

糖尿病视网膜病变(DR)是糖尿病(DM)最常见的微血管慢性并发症之一，其发病机制复杂，一直是国内外的研究热点之一。神经退行性病变、炎症和血管交替的再生与损伤共同促进DR的发生发展。近年来，越来越多的证据表明，视网膜的慢性低度炎症是DR的一个关键因素，是DR更为早期的表现，然而确切的分子机制尚不完全清楚。本文就炎症在DR发病机制中的作用及干预机制进行综述。     

环状RNA在眼底疾病中的研究进展

环状RNA（circRNA）是一类通过反向剪接生成的新的内源性非编码RNA,具有miRNA"海绵"、调节转录和剪接、调节蛋白之间的相互作用等功能。最近的研究表明,circRNA在视网膜微血管功能障碍、糖尿病视网膜病变、老年性黄斑变性、增生性玻璃体视网膜病变、高同型半胱氨酸血症所致眼病和眼部恶性肿瘤等眼底疾病的发生和发展...     

昼夜节律和生物钟基因与糖尿病视网膜病变发病的相关性研究进展

糖尿病视网膜病变(diabetic retinopathy, DR)是糖尿病患者最常见的微血管并发症,已成为全球工作年龄人群视力障碍的主要原因之一。DR的发生是多种机制共同作用的结果,越来越多的研究表明昼夜节律及生物钟基因与DR的发病密切相关。昼夜节律是受生物钟基因调控,以24h为周期,与外界明暗变化相一致的生理过程,生物钟调控机体的各种生理活动。昼夜节律紊乱通过影响糖尿病患者的血糖水平和眼部的生理稳态等诱导DR的发生,生物钟基因可能通过调控DR的氧化应激反应、炎症反应、视网膜自噬节律、线粒体功能障碍以及内皮祖细胞功能等各方面参与DR的发病。本文介绍了昼夜节律的产生及调控机制,以及视网膜内在昼夜节律生物钟,深入探讨了昼夜节律系统以及生物钟基因在DR发生发展过程中的影响,旨在为DR的预防及治疗提供参考。     

长链非编码RNA在糖尿病视网膜病变发病机制中的作用

糖尿病视网膜病变(diabetic retinopathy,DR)是一种严重的糖尿病微血管并发症,是糖尿病患者失明的主要原因之一。长链非编码RNA(long non-coding RNA,lncRNA)是一类核苷酸数大于200且不编码蛋白质的RNA,在多种生理和病理过程中发挥重要作用。最新研究表明,在糖尿病及其相关微血管并发症中广泛存在lncRNA的异常表达。本文将对目前DR相关lncRNA的基因组起源以及其在DR发生发展中的分子机制及调控作用进行综述,并讨论lncRNA在DR诊断和治疗中的前景。     

小胶质细胞在糖尿病视网膜病变视网膜神经血管单元中的作用

糖尿病视网膜病变(DR)是工作年龄人群主要致盲眼病,血-视网膜屏障破坏是关键环节。近年研究显示,DR不再是单纯微血管病变,而是视网膜胶质细胞与神经退行性变、微血管病变的共同发展结果。DR病程早期视网膜神经血管单元(RNVU)中神经元的损伤可能早于血管内皮的变化,胶质细胞的激活加重血管屏障功能障碍。视网膜小胶质细胞是常驻视网膜的局部免疫细胞,参与长期高糖诱导的慢性炎症反应、高糖诱导其分泌多种炎症因子,破坏血-视网膜屏障结构、增加神经元凋亡、改变Müller细胞胶质化等,影响视网膜局部稳态平衡。RNVU作为一个单元结构研究,近年来受到越来越多的关注,本文将针对小胶质细胞在RNVU中的作用机制、研究进展进行综述。     

巨噬细胞在糖尿病视网膜病变中的作用

糖尿病视网膜病变(diabetic retinopathy,DR)是糖尿病常见且严重的微血管并发症,是视力损害的重要原因之一,其发生和发展是一个多细胞参与,多因素调控的复杂过程.巨噬细胞来源于单核细胞,是视网膜主要的炎性细胞,参与视网膜的许多病理和生理过程.随着越来越多的研究着眼于DR病程中炎症的作用,人们发现巨噬细胞对DR的发病机制研究有着重要意义.     

IL-8与糖尿病视网膜病变

糖尿病视网膜病变(diabetic retinopathy,DR)是最常见的糖尿病微血管并发症之一,然而其具体机制尚不清楚。现在炎症反应作为DR发病机制之一而被越来越多的学者关注,并提出DR是一种炎症性疾病。我们就炎症因子IL-8的特征及其在DR发生发展过程中的作用加以综述。     

Strabisme Alternant - Etude clinique - traitement

The author defines motor and sensory alternation: the term alternation should not be used in isolation, it should always be accompanied by the name of the parameter concerned. Sensory alternation is always found together with motor alternation but the reverse is not true.The examining criteria for a diagnosis of sensory alternation are given, sensory alternation must not be confused with alternating inhibition. Working from clinical observations of cases of motor alternating strabismus, the author selects 2 types of binocular sensory relations which allow one to differentiate between:- cases of primary alternating strabismus- cases of secondary alternating strabismusThese forms will develop in different ways; in both cases a cure is possible providing that the right treatment is prescribed and once prescribed carefully followed, etc. It is always a case of serious forms of strabismus whose developmental period is spread over several years.According to the authors, the frequency of cases of true primary strabismus is from 1–3%, the frequency of cases of secondary alternating strabismus varies according to the type of therapy practised on cases of monocular strabismus with amblyopia. These latter will become cases of alternating strabismus under the influence of certain types of therapy carried out over several years (penalization, rocking, alternated occlusion, etc...).Experimental data on kittens confirm clinical data; kittens placed in abnormal environments during the sensitive period will show modification in the distribution of cortical cells and the absence of binocular cells (either because the excitation of the two eyes was not simultaneous, or not identical: artificial strabismus, occlusion, opaque glasses). This disturbances become irreversible after a certain period of exposure (a function of age, length of exposure, etc...).It is thus necessary to bear in mind: 1) the iatrogenic risks of certain orthoptic treatments, 2) the necessity for a binocular form of treatment as soon as possible, as once a certain stage is passed, cortical plasticity diminishes and the elaboration of normal binocular relations becomes impossible.

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Effects of Adenosine Agonists on Intraocular Pressure and Aqueous Humor Dynamics in Cynomolgus Monkeys

The effects of single or multiple topical doses of the relatively selective A₁adenosine receptor agonists (R)-phenylisopropyladenosine (R-PIA) and N⁶-cyclohexyladenosine (CHA) on intraocular pressure (IOP), aqueous humor flow (AHF) and outflow facility were investigated in ocular normotensive cynomolgus monkeys. IOP and AHF were determined, under ketamine anesthesia, by Goldmann applanation tonometry and fluorophotometry, respectively. Total outflow facility was determined by anterior chamber perfusion under pentobarbital anesthesia. A single unilateral topical application of R-PIA (20–250 μg) or CHA (20–500 μg) produced ocular hypertension (maximum rise=4.9 or 3.5 mmHg) within 30 min, followed by ocular hypotension (maximum fall=2.1 or 3.6 mmHg) from 2–6 hr. The relatively selective adenosine A₂antagonist 3,7-dimethyl-1-propargylxanthine (DMPX, 320 μg) inhibited the early hypertension, without influencing the hypotension. Neither 100 μg R-PIA nor 500 μg CHA clearly altered AHF. Total outflow facility was increased by 71% 3 hr after 100 μg R-PIA. In conclusion, the early ocular hypertension produced by topical adenosine agonists in cynomolgus monkeys is associated with the activation of adenosine A₂receptors, while the subsequent hypotension appears to be mediated by adenosine A₁receptors and results primarily from increased outflow facility.