Diabetic retinopathy (DR) is one of common and specific microvascular complications caused by diabetic mellitus, and remains a serious and common ocular complication leading preventable blindness. At present, the specific pathogenesis of DR is not completely clear, and many factors are involved in its occurrence and development. Adiponectin (APN) is an endogenous cytokine secreted by adipocytes. It is expressed in all layers of retina, especially in the outer layer (rods and cones). It is involved in regulating fatty acid oxidation and glucose metabolism by binding with specific receptors. In recent years, a lot of studies have found that APN can be involved in regulating blood glucose, inhibiting neovascularization, reducing inflammation, dilating blood vessels and improving vascular endothelial function. At present, the specific mechanism of APN in the occurrence and development of DR Remains to be determined. Further research on the level changes and the specific mechanism of action of APN in DR may help to identify the characteristic metabolic changes of DR, thus providing new biomarkers for the diagnosis of DR, while helping to promote the innovation of the treatment of DR.
Diabetic retinopathy (DR), a neurovascular complication of diabetes, presents a multifaceted pathogenesis that encompasses numerous biological processes and molecular mechanisms. Endoplasmic reticulum stress (ERS) plays a critical role in the maintenance of cellular homeostasis, and diabetic neuro-microangiopathy is driven by high glucose, which activated ERS through the promotion of protein misfolding, oxidative stress, and disturbances in calcium homeostasis. ERS activates the unfolded protein response, thereby influencing the onset and progression of DR through modulating mitochondria-associated endoplasmic reticulum membranes, autophagy, apoptosis, microvascular function, oxidative stress, and inflammation pathways. Currently, the principal interventions against ERS comprise the modulation of the ERS signalling axis and its interactions with associated pathological processes such as autophagy, oxidative stress, and inflammation, through pharmacological and molecular mechanisms. These interventions are directly or indirectly shown to inhibit persistent ERS and are demonstrated to ameliorate DR. With the in-depth study of ERS and the research and development of various drugs for ERS, it is expected to bring novel insights and strategies for DR management in the future.
Objective To observe the changes of retinal nerve fiber layer (RNFL) thickness in patients with Alzheimer's disease (AD). Methods Twenty eyes of 40 patients with mild and (or) moderate AD confirmed by clinical examination (AD group) were included in the study. There were 11 males and 9 females with an average age of (72.75±8.25) years. Age and gender-matched normal 20 objectives were in the normal control group. Among them, there were 11 males and 9 females with a mean age of (71.05±7.08) years. There was no significant difference in gender composition, age and intraocular pressure between the two groups (P＞0.05). There were significant differences in visual acuity, cup disc ratio and mini-mental state examination score (P＜0.05). All eyes underwent high-resolution optical coherence tomography (OCT) examination. With a diameter of 3.4 mm and a center on the center of the optic disc, circular fast scans on optic disc were performed to obtain an average disc RNFL thickness, signal threshold ＞6. Computer image analysis system was used to measure the RNFL thickness from superior, inferior, temporal and nasal quadrants, and the average RNFL thickness. The changes of RNFL thickness between the two groups and between different eyes of the same group were compared. Results Compared with the normal control group, the average (t=5.591), superior (t=8.169, 8.053) and inferior (t=12.596, 11.377) thickness of RNFL in both eyes in AD group were thinner, the differences were significant (P＜0.05); the temporal (t=1.966, 0.838）and nasal (t=2.071, 0.916) thickness of RNFL in both eyes of AD group were thinner, but the difference was not statistically significant (P＞0.05). There was no significant difference of the mean and different quadrant RNFL thickness between different eyes in AD group and normal control group (AD group: t=0.097, 0.821, 0.059, 0.020, 0.116; normal control group: t=0.791, 1.938, 1.806, 2.058, 1.005; P＞0.05). Conclusion The RNFL thickness around the optic disc in AD patients is thinner; This occurs first in superior and inferior quadrants of the optic disc.