Epilepsy is one of the most common neurological disorders, and status epilepticus (SE) can lead to permanent neuronal brain damage in the central nervous system, but the mechanism is not clear. Solving this problem will help to find more SE therapeutic targets, benefiting tens of millions of epilepsy patients. The pathway of SE leading to neuronal damage in the brain has made new progress in neuroinflammation, autophagy, apoptosis and pyroptosis, glial cell hyperplasia and category transformation, and changes in neurotransmitters in the brain, which will be beneficial to the discovery of new targets for the treatment of SE, thus laying a foundation for the development of new anti-epileptic drugs.
ObjectiveTo summarize the therapeutic targets of pancreatic cancer (PC). MethodsThe related literatures about the therapeutic targets of PC were reviewed. ResultsPC was one of the most challenging tumor in worldwide, and was characterized as a highly aggressive disease with poor overall prognosis and a high mortality rate. The hallmark of PC was its poor response to radio-and chemo-therapy. Current chemotherapeutic regimens could not provide substantial survival benefit with a clear increase in overall survival. Recently, several new approaches which could significantly improve the clinical outcome of PC had been described, involving signal-transduction pathways, immune response, stroma reaction, and epigenetic changes. ConclusionsMany therapeutic targets are involved in the treatment of PC. As current therapies failed to significantly improve the progression and the survival of PC, new therapeutic approaches and clinical studies are strongly required.
Retinopathy of Prematurity (ROP) is a blinding eye disease characterized by abnormal retinal vascular proliferation and is a major cause of visual impairment in children. Its pathogenesis is complex, involving multiple factors such as hyperoxia exposure, hypoxic compensation, oxidative stress, inflammatory responses, and abnormal angiogenesis, with oxidative stress playing a central role. It is characterized by excessive production of reactive oxygen species and impaired antioxidant function, leading to retinal vascular endothelial cell damage, formation of avascular areas, and abnormal vascular proliferation. Studies have shown that oxidative stress can promote the development and progression of ROP through vascular damage, nitrooxidative stress synergy, and interference with cellular metabolism. Current treatment strategies mainly include antioxidant agents (such as vitamin C, vitamin E, and lutein), signal pathway regulatory agents (such as nuclear factor erythroid 2-related factor 2 activators, signal transducer and activator of transcription 3 inhibitors), corticosteroids (such as Triamcinolone and Dexamethasone), and adrenergic receptor antagonists (such as Propranolol), but their efficacy and safety still require further validation. In the future, multidisciplinary collaboration should be strengthened to further explore the interactions between oxidative stress and other pathological mechanisms, and long-term follow-up studies should be conducted to develop safer and more effective strategies for the prevention and treatment of ROP, thereby improving the visual outcomes of preterm infants.
Diabetic retinopathy (DR) is one of the most common microvascular complications of diabetes, characterized by high blindness rates and a severe impact on patients' quality of life. Despite adequate glycemic control, some patients exhibit persistent progression of retinal microvascular damage, known as the "metabolic memory" phenomenon. Studies have revealed that the essence of this phenomenon is the sustained expression of epigenetic reprogramming induced by metabolic stress, in which abnormal mitochondrial DNA (mtDNA) methylation plays a pivotal role. Metabolic abnormalities such as hyperglycemia, hyperhomocysteinemia, and hyperlipidemia can alter mtDNA methylation patterns, triggering cascading pathological processes including oxidative stress, chronic inflammation, and neurovascular network disorders, remodeling mitochondrial energy metabolism, and promoting the evolution of DR from subclinical compensatory stage to irreversible structural damage. Abnormal mtDNA methylation serves as a hallmark of metabolic memory and a core driver of microvascular lesions, providing an important theoretical basis for in-depth analysis of metabolic memory mechanisms and exploration of DR intervention strategies. Current research needs to further elucidate its role in DR. Future efforts require integration of multi-dimensional epigenetic biomarkers, precise intervention approaches, and clinical translational research to advance the early diagnosis and individualized treatment of DR.