The reattachment rate, macular hole (MH) closure rate, visual acuity improvement and re-detachment rate of MH retinal detachment (MHRD) of high myopia are not satisfactory owing to long axis oculi, posterior scleral staphyloma and macular atrophy. At present, minimally invasive vitrectomy surgery combined with the internal limiting membrane flap technique has become popular in the treatment of MHRD, as it can promote MH closure, and significantly improve the outcome of MHRD. However if this method can improve the postoperative visual function is still controversial. The advantage of this technique is that the loosened internal limiting membrane is applied to cover the MH surface to form a scaffold structure similar to the basement membrane. It can stimulate Müller cell gliosis more effectively, and promote tissue filling in the MH which results in MH closure. It can also promote retinal reattachment and reduce the likelihood of retinal re-detachment. This technique is expected to be a standard surgical method for the treatment of MHRD of high myopia in the future. The inserted internal limiting membrane flap technique is relatively easy to perform, induces stable flaps by simple procedures, and can be an essential complement procedure of the inverted internal limiting membrane flap technique. In order to reduce the recurrence rate in the future, it is necessary to further define the indications of different surgical methods and the predictive effects of MH healing mode on the success rate and visual function recovery.
Pyroptosis is a newly discovered form of cell death. Through the activation of inflammasome complexes, pyroptosis induces the production of interleukin (IL) -1β and IL-18, and the osmotic swelling of cells, thus induces cellular rupture and death. It plays a role in the pathological process of a variety of human diseases. The death of retinal cells including photoreceptor cells and retinal pigment epithelium (RPE) cells is the main reason leading to visual dysfunction in the pathogenesis in ocular fundus diseases. Researches have demonstrated that pyroptosis is closely related to the onset and progression of various retinal diseases. In age-related macular degeneration, pyroptosis directly causes apoptosis of RPE cells and upregulation of pro-inflammatory factors, enhancing toxic effect of lipofuscin. For retinitis pigmentosa, pyroptosis is the leading manner of death of secondary cone photoreceptor cells. In cytomegalovirus retinitis, pyroptosis is the main responding way to infection. This review presented the molecular mechanism of pyroptosis and its role in age-related macular degeneration, retinitis pigmentosa and cytomegalovirus retinitis and other retinal diseases.
Diabetic retinopathy (DR), which is a common complication of diabetic and the main cause of blindness, brings not only a heavy economic burden to society, but also seriously threatens to the patients’ quality of life. Clinical researches on the therapies of DR are active at present, but how to perform a good clinical research with scientific design should be considered with high priority. The randomized controlled trial (RCT) is considered to be the gold standard for evidence-based medicine, but RCT is not always perfect. Limitations still exist in certain circumstance and the conclusions from RCTs also need to be interpreted by an objective point of view before clinical practice. Real world study (RWS) bridges the gap between RCT and clinical practice, in which the data can be easily collected without much cost, and results might be obtained within a short period. However, RWS is also faced with the challenge of not having standardized data and being susceptible to confounding bias. The standardized single disease database for DR and propensity score matching method can provide a wide range of data sources and avoid of bias for RWS in DR.
Photoreceptor cells are special retinal neurons with photo-transformation ability. Loss of photoreceptors in age-related macular degeneration (AMD) is secondary to RPE loss, leakage of serum components from the neovascularization and scar formation, which is one of the main mechanisms of irreversible visual impairment in patients with AMD. Many studies have shown that inflammatory environment is involved in the process of photoreceptor cell death. Aging, photooxidation injury and other factors affects the retinal microenvironment through different levels of mechanisms such as retinal pigment epithelial cells, retinal glial cells, hematogenous macrophages and inflammatory factors, which results in photoreceptor injuries and participates in the progression of AMD by drusen formation and neovascularization. This study reviews the research status and progress of inflammation and photoreceptor cell death, and provides new ideas for exploring the blinding mechanism and treatment strategies of AMD.
Age-related macular degeneration (AMD) is an age-related degenerative disease with complex pathogenesis, whose initial lesion is accompanied with immune inflammatory response. Amyloid beta (Aβ), a small-molecule protein generated by the hydrolysis of amyloid precursor protein, as the main component, is involved in the formation of drusen, which serves as the early characteristic of AMD. In the local inflammatory response of AMD, Aβ is an important pathological deposit, promoting the proliferation and differentiation of macrophages as well as changing their morphology to accelerate the progression of AMD. In addition, Aβ can also regulate immune molecules and the complement system by activating inflammatory pathways, thus mediating chronic retinal inflammation and promoting the course of AMD. However, since AMD is not caused by inflammation alone, only the immunosuppression may not be effective in inhibiting the course of AMD, and thus the future development is to rebalance the disordered immune system in AMD patients eyes.
The application of gene therapy in ocular diseases is gradually expanding from mono-gene inherited diseases to multigene, multifactorial, common and chronic diseases. This emerging therapeutic approach is still in the early exploratory stage of treating diseases, and the expected benefits and risks remain highly uncertain. In the delivery process of gene therapy drugs, viral vector is currently one of the most mature and widely used vectors. The occurrence of vector-associated immunity will affect the short-term and long-term effects of gene therapy, and even cause permanent and serious damage to visual function. Therefore, gene therapy vector-associated immunity is the focus and challenge for the safety and long-term efficacy of gene therapy. During the perioperative and follow-up of gene therapy, attention should be paid to the monitoring of vector-associated immune inflammation, and appropriate measures should be taken to deal with the corresponding immune response, so as to achieve the best visual benefits for patients.
Serum anti-retinal autoantibodies (ARA) are a group of autoantibodies that bind to retinal auto-antigens with significant biological importance in pathological processes such as retinal degeneration, inflammatory microenvironment formation, and tissue destruction. In recent years, the expression of serum anti-retinal antibodies has been found to be upregulated in patients with various blinding retinal diseases such as age-related macular degeneration, autoimmune retinopathy, and retinitis pigmentosa, closely correlated with the progression of diseases. However, current researches on ARA are incomplete, lacking animal experiments and large randomized controlled clinical trials. As a result, the exact mechanism of ARA is not well understood. Although several studies have demonstrated that serum ARA has an important diagnostic value in hereditary, autoimmune, and degenerative retinal diseases, there still lacks recognized laboratory tests and laboratory indicators with high specificity and sensitivity. Clinical symptoms should be considered when making definitive diagnosis of the diseases. Therefore, clarifying the mechanisms of ARA in retinal dystrophies provides new ideas in early diagnosis and treatments of retinal diseases, which is clinically and scientifically important for the maintenance of visual functions.
ObjectiveTo observe the clinical efficacy of vitrectomy combined with modified inverted internal limiting membrane (ILM) flap covering technique for complicated macular hole (MH).MethodsThis is a retrospective case series. Twenty-one eyes of 20 patients who underwent vitrectomy combined with modified inverted ILM flap covering technique were enrolled in this study. Among these eyes, 9 eyes were idiopathic MH (IMH), with the mean basal diameter of (1 188.3±155.1) μm, minimum diameter of (626.9±86.2) μm, logarithm of the minimum angle of resolution (logMAR) best corrected visual acuity (BCVA) of 1.1±0.3; 2 eyes were MH with high myopia, with the mean basal diameter of (696.5±232.6) μm, minimum diameter of (259.0±69.3) μm, logMAR BCVA of 1.3; 5 eyes were high myopia MH with retinal detachment (RD), with the mean BCVA of 1.5±0.1; 3 eyes were rhegmatogenous RD (RRD) with MH, with the mean logMAR BCVA of 1.6; 2 eyes were MH after vitrectomy for RRD, with the mean basal diameter of (1 606.0±69.3) μm, minimum diameter of (909.0±387.5) μm, logMAR BCVA of 1.6. All patients received 23G or 25G vitrectomy after removal of posterior vitreous cortex intraoperatively. Indocyanine green staining assisted circle-wise ILM peeling was performed. ILM of diameter 1.5 disc-diameters around fovea was residual and loosened; perfluoronoctane assisted inverting superior or temporal residual ILM covering on macular hole. C3F8, gas or silicone oil tamponade was performed at the end. BCVA and hole closure were followed up for 1-4 months. C3F8, gas or silicone oil was tamponaded at the end. BCVA and hole closure were followed up for 1-4 months.ResultsMH of 21 eyes were closed after surgery. Nine IMH were closed at typeⅠ, with U shape closure in 7 eyes, V shape closure in 2 eyes. Two eyes of MH with high myopia, 3 eyes of RRD with MH, 2 eyes of MH after vitrectomy for RRD were closed at typeⅠ of U shape. Five eyes of high myopia MHRD including MH closure at typeⅠof U shape 3 eyes, typeⅡ of W shape 2 eyes. The mean logMAR BCVA of IMH, MH with high myopia, high myopia MHRD, RRD with MH, MH after vitrectomy for RRD eyes were 0.8±0.3, 0.9±0.2, 1.4±0.1, 0.7±0.3, 0.9±0.2, respectively. The mean postoperative logMAR BCVA in IMH eyes was improved compared preoperative one (P=0.02). There was no obvious change of pre-and postoperative logMAR BCVA in MH with high myopia, high myopia MHRD, RRD with MH, MH after vitrectomy for RRD eyes (P=0.18, 0.10, 0.11, 0.18).ConclusionVitrectomy combined with inverted ILM flap covering technique for complicated MH is an effective method to improve the success rate of MH closure and the visual function.
Exudative or wet age-related macular degeneration (AMD) is characterized by the progressive growth of choroidal neovascularization (CNV). Anti-vascular endothelial growth factor (VEGF) drugs have been used in the control of the development of CNV and vision improvement, but there are still defects like frequent injections, drug resistance and so on. Radiotherapy can deactivate local inflammatory cell populations, and make CNV unstable in the absence of pericytes and VEGF stimulation, which induce apoptosis of the vascular endothelial cells. Therefore, radiotherapy is considered as a potential adjuvant treatment of anti-VEGF therapy. The current clinical approaches include epimacular brachytherapy (EMBT) and long-range stereotactic radiotherapy (SRT). SRT may be a preferred adjuvant treatment for patients receiving anti-VEGF therapy. Knowing the progress of radiotherapy for the treatment of exudative AMD may help us to fully understand the pathogenesis of wAMD in China
Age-related macular degeneration is one of the major causes of blindness in the elderly. As an important pathway of cell metabolism, autophagy maintains intracellular homeostasis through the degradation and recycle of damaged organelles and macromolecules. Understanding its mechanism may promote discoveries to delay aging process, reduce the incidence of age-related diseases. In mammals, silent information regulator protein 6 (SIRT6) plays its deacetylase and ribonucleotransferase activity in multiple signaling pathways, including inhibition of cellular senescence, tumorigenesis, metabolic diseases, regulating cellular lifespan. It has a significant impact on the structure and function of tissues and organs. SIRT6 regulates intracellular autophagy mainly through the insulin-like growth factor-protein kinase B-mammalian target of rapamycin, reducing the accumulation of toxic metabolites and cellular senescence. The function of SIRT6 in age-related macular degeneration need to be combined with the genetic background, pathogenesis, clinical manifestations and other aspects of the disease, and it is expected to be further studied in subsequent studies.