10
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Autophagy in the retinal neurovascular unit: New perspectives into diabetic retinopathy Translated title: 视网膜神经血管单元自噬:糖尿病视网膜病变的新视角

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Diabetic retinopathy (DR) is one of the most prevalent retinal disorders worldwide, and it is a major cause of vision impairment in individuals of productive age. Research has demonstrated the significance of autophagy in DR, which is a critical intracellular homeostasis mechanism required for the destruction and recovery of cytoplasmic components. Autophagy maintains the physiological function of senescent and impaired organelles under stress situations, thereby regulating cell fate via various signals. As the retina's functional and fundamental unit, the retinal neurovascular unit (NVU) is critical in keeping the retinal environment's stability and supporting the needs of retinal metabolism. However, autophagy is essential for the normal NVU structure and function. We discuss the strong association between DR and autophagy in this review, as well as the many kinds of autophagy and its crucial physiological activities in the retina. By evaluating the pathological changes of retinal NVU in DR and the latest advancements in the molecular mechanisms of autophagy that may be involved in the pathophysiology of DR in NVU, we seek to propose new ideas and methods for the prevention and treatment of DR.

          Abstract

          Highlights

          Autophagy is closely related to retinal neurovascular units in diabetes retinopathy. Different cells participate in the occurrence and development of diseases through autophagy, and targeted autophagy may be a new direction of treatment in the future.

          • Emphasized the close relationship between diabetic retinopathy (DR) and autophagy

          • Summarized the autophagy molecular mechanism of DR pathophysiology in the neurovascular unit

          • Proposed potential targets for DR treatment

          摘要

          糖尿病视网膜病变(DR)是世界范围内最常见的视网膜疾病之一,是育龄人群视力损害的主要原因。研究表明,自噬是破坏和恢复胞质成分所需的一种重要的细胞内稳态机制,在DR中具有重要意义。自噬维持应激状态下衰老和受损细胞器的生理功能,从而通过多种信号调节细胞寿命。视网膜神经血管单元(NVU)作为视网膜的基本功能单位,在维持视网膜环境稳定和支持视网膜代谢需求方面起着至关重要的作用。然而,自噬对于NVU的正常结构和功能至关重要。本文就DR与自噬的密切关系、自噬的种类及其在视网膜中的重要生理活性进行综述。我们期望通过评估DR中视网膜NVU的病理变化以及自噬可能参与NVU中DR病理生理分子机制的最新进展,寻求防治DR的新思路和方法。

          Related collections

          Most cited references126

          • Record: found
          • Abstract: found
          • Article: not found

          A role for mitochondria in NLRP3 inflammasome activation.

          An inflammatory response initiated by the NLRP3 inflammasome is triggered by a variety of situations of host 'danger', including infection and metabolic dysregulation. Previous studies suggested that NLRP3 inflammasome activity is negatively regulated by autophagy and positively regulated by reactive oxygen species (ROS) derived from an uncharacterized organelle. Here we show that mitophagy/autophagy blockade leads to the accumulation of damaged, ROS-generating mitochondria, and this in turn activates the NLRP3 inflammasome. Resting NLRP3 localizes to endoplasmic reticulum structures, whereas on inflammasome activation both NLRP3 and its adaptor ASC redistribute to the perinuclear space where they co-localize with endoplasmic reticulum and mitochondria organelle clusters. Notably, both ROS generation and inflammasome activation are suppressed when mitochondrial activity is dysregulated by inhibition of the voltage-dependent anion channel. This indicates that NLRP3 inflammasome senses mitochondrial dysfunction and may explain the frequent association of mitochondrial damage with inflammatory diseases.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: found
            Is Open Access

            Global Prevalence and Major Risk Factors of Diabetic Retinopathy

            OBJECTIVE To examine the global prevalence and major risk factors for diabetic retinopathy (DR) and vision-threatening diabetic retinopathy (VTDR) among people with diabetes. RESEARCH DESIGN AND METHODS A pooled analysis using individual participant data from population-based studies around the world was performed. A systematic literature review was conducted to identify all population-based studies in general populations or individuals with diabetes who had ascertained DR from retinal photographs. Studies provided data for DR end points, including any DR, proliferative DR, diabetic macular edema, and VTDR, and also major systemic risk factors. Pooled prevalence estimates were directly age-standardized to the 2010 World Diabetes Population aged 20–79 years. RESULTS A total of 35 studies (1980–2008) provided data from 22,896 individuals with diabetes. The overall prevalence was 34.6% (95% CI 34.5–34.8) for any DR, 6.96% (6.87–7.04) for proliferative DR, 6.81% (6.74–6.89) for diabetic macular edema, and 10.2% (10.1–10.3) for VTDR. All DR prevalence end points increased with diabetes duration, hemoglobin A1c, and blood pressure levels and were higher in people with type 1 compared with type 2 diabetes. CONCLUSIONS There are approximately 93 million people with DR, 17 million with proliferative DR, 21 million with diabetic macular edema, and 28 million with VTDR worldwide. Longer diabetes duration and poorer glycemic and blood pressure control are strongly associated with DR. These data highlight the substantial worldwide public health burden of DR and the importance of modifiable risk factors in its occurrence. This study is limited by data pooled from studies at different time points, with different methodologies and population characteristics.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Microglial M1/M2 polarization and metabolic states.

              Microglia are critical nervous system-specific immune cells serving as tissue-resident macrophages influencing brain development, maintenance of the neural environment, response to injury and repair. As influenced by their environment, microglia assume a diversity of phenotypes and retain the capability to shift functions to maintain tissue homeostasis. In comparison with peripheral macrophages, microglia demonstrate similar and unique features with regards to phenotype polarization, allowing for innate immunological functions. Microglia can be stimulated by LPS or IFN-γ to an M1 phenotype for expression of pro-inflammatory cytokines or by IL-4/IL-13 to an M2 phenotype for resolution of inflammation and tissue repair. Increasing evidence suggests a role of metabolic reprogramming in the regulation of the innate inflammatory response. Studies using peripheral immune cells demonstrate that polarization to an M1 phenotype is often accompanied by a shift in cells from oxidative phosphorylation to aerobic glycolysis for energy production. More recently, the link between polarization and mitochondrial energy metabolism has been considered in microglia. Under these conditions, energy demands would be associated with functional activities and cell survival and thus, may serve to influence the contribution of microglia activation to various neurodegenerative conditions. This review examines the polarization states of microglia and their relationship to mitochondrial metabolism. Additional supporting experimental data are provided to demonstrate mitochondrial metabolic shifts in primary microglia and the BV-2 microglia cell line induced under LPS (M1) and IL-4/IL-13 (M2) polarization.
                Bookmark

                Author and article information

                Contributors
                caomzh7@mail.sysu.edu.cn
                yigg@mail.sysu.edu.cn
                min_fu1212@163.com
                Journal
                J Diabetes
                J Diabetes
                10.1111/(ISSN)1753-0407
                JDB
                Journal of Diabetes
                Wiley Publishing Asia Pty Ltd (Melbourne )
                1753-0393
                1753-0407
                02 March 2023
                May 2023
                : 15
                : 5 ( doiID: 10.1111/jdb.v15.5 )
                : 382-396
                Affiliations
                [ 1 ] Zhujiang Hospital Southern Medical University Guangzhou Guangdong P. R. China
                [ 2 ] The Second Clinical School Southern Medical University Guangzhou Guangdong P. R. China
                [ 3 ] The Second People's Hospital of Jingmen Jingmen Hubei People's Republic of China
                [ 4 ] Department of Ophthalmology, Zhujiang Hospital Southern Medical University Guangzhou Guangdong P. R. China
                [ 5 ] Department of Ophthalmology, The Seventh Affiliated Hospital Sun Yat‐Sen University Shenzhen P. R. China
                [ 6 ] Department of Ophthalmology, The Sixth Affiliated Hospital Sun Yat‐Sen University Guangzhou Guangdong P. R. China
                Author notes
                [*] [* ] Correspondence

                Mingzhe Cao, Department of Ophthalmology, The Seventh Affiliated Hospital, Sun Yat‐Sen University, Shenzhen, P. R. China.

                Email: caomzh7@ 123456mail.sysu.edu.cn

                Guoguo Yi, Department of Ophthalmology, The Sixth Affiliated Hospital, Sun Yat‐Sen University, No. 26, Erheng Road, Yuancun, Tianhe, Guangzhou, Guangdong, P. R. China.

                Email: yigg@ 123456mail.sysu.edu.cn

                Min Fu, Department of Ophthalmology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, P. R. China.

                Email: min_fu1212@ 123456163.com

                Author information
                https://orcid.org/0000-0003-2638-1756
                Article
                JDB13373
                10.1111/1753-0407.13373
                10172025
                36864557
                cf3f1863-2768-426b-8952-ce10306b2a10
                © 2023 The Authors. Journal of Diabetes published by Ruijin Hospital, Shanghai JiaoTong University School of Medicine and John Wiley & Sons Australia, Ltd.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 08 February 2023
                : 12 December 2022
                : 18 February 2023
                Page count
                Figures: 5, Tables: 0, Pages: 15, Words: 11272
                Categories
                Review Article
                Review Articles
                Custom metadata
                2.0
                May 2023
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.2.8 mode:remove_FC converted:10.05.2023

                Endocrinology & Diabetes
                autophagy,diabetic retinopathy,mitophagy,retinal neurovascular unit,自噬,糖尿病性视网膜病变,线粒体自噬,视网膜神经血管单元

                Comments

                Comment on this article