Objective To realize the research progress of regulating the endoplasmic reticulum stress response to inhibit autophagy in tumor cells. Method The literatures about regulating the endoplasmic reticulum stress response to inhibit autophagy in tumor cells were reviewed. Result In the endoplasmic reticulum stress response induced by the release of calcium and accumulation of unfolded proteins, autophagy can be activated by several pathways, and to regulate physiological and pathological processes. Conclusion Further research about the endoplasmic reticulum stress response in tumor cells need to be done to regulate the response factors to inhibit autophagy.
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.
The occurrence and development of myopia is closely related to scleral remodeling. Therefore, in order to effectively prevent and cure myopia, it is very important to clarify the mechanism of scleral remodeling. In recent years, Chinese scholars have found that endoplasmic reticulum stress can regulate the expression of apoptotic proteins through the inositol demand protein-1/X box binding protein-1 pathway in the unfolded protein response, thus it is involved in regulating the state of scleral fibroblasts under hypoxia and regulating the occurrence and development of scleral remodeling. At the same time, some studies have found that inhibiting and knocking out protein kinase RNA-like endoplasmic reticulum kinase and activated transcription factor 6 in endoplasmic reticulum stress can effectively inhibit the growth of ocular axis. This proves that endoplasmic reticulum stress plays an important role in the occurrence and development of scleral remodeling. However, the comprehensive analysis of endoplasmic reticulum stress and scleral remodeling has not been reported at home and abroad. In-depth analysis of the relationship between endoplasmic reticulum and scleral remodeling is of great significance for the follow-up analysis and study of the mechanism of scleral remodeling.
