Immunoglobulin A nephropathy (IgAN) is an immune-mediated chronic inflammatory disease with a complex pathogenesis and diverse clinical manifestations. Currently, there is no specific treatment plan. Programmed cell death is an active and orderly way of cell death controlled by genes in the body, which maintains the homeostasis of the body and the development of organs and tissues by participating in various molecular signaling pathways. In recent years, programmed cell death has played an important regulatory role in the occurrence and development of IgAN, involving complex signaling pathways. Under pathological conditions, it may relieve kidney damage through various pathways such as reducing oxidative stress, inhibiting inflammation, and improving energy metabolism. This article provides a review of the research progress of IgAN in apoptosis, autophagy, pyroptosis, ferroptosis,and cuproptosis in order to provide new therapeutic targets for IgAN.
ObjectiveTo summarize the latest advances in copper and cuproptosis in the field of breast cancer, and to provide a reference for clinical treatment decisions. MethodThe literatures related to copper and cuproptosis in recent years were read and summarized, and the research progress on the role of copper in breast cancer, the application of cuproptosis in the diagnosis and treatment of breast cancer were reviewed. ResultsCuproptosiswas a novel form of programmed cell death, which occurred via direct binding of copper to lipoylated components of the tricarboxylic acid (TCA) cycle, this resulted in lipoylated protein aggregation and subsequent iron-sulfur cluster protein loss, leading to proteotoxic stress and ultimately cell death. Cuproptosis induced proliferation and migration of breast cancer cell , mediated personalized immunotherapy, and participated in endocrine and chemotherapeutic drug resistance. ConclusionExploring the mechanism of cuproptosis provides potential applications for subsequent immunotherapy, endocrine therapy, and chemotherapy for breast cancer, leading to new effective strategies for patients.
Cuproptosis, recently defined as a unique form of cell death distinct from programmed cell death, is triggered by copper overload within mitochondria. Genes associated with cuproptosis have been found to correlate with tumorigenesis and tumor progression, making the targeting of cuproptosis pathways a promising direction for anti-tumor therapies. Copper ion carriers can transport copper ions into cells, inducing cuproptosis and laying the foundation for its application in cancer treatment. This article elaborates on the homeostasis of copper and the mechanisms related to cuproptosis, further clarifying the relationship between cuproptosis and lung cancer treatment targets. This review aims to summarize current progress in research related to cuproptosis and lung cancer, providing new theories and bases for the clinical treatment of lung cancer.
ObjectiveObjective To summarize the latest research progress on the copper death mechanism in metabolic associated fatty liver disease (MAFLD) and to provide new avenues for the treatment of MAFLD. MethodsWe reviewed recent domestic and international research on copper and copper death in MAFLD, and summarized the role of copper death mechanisms in the pathogenesis of MAFLD and related treatments. ResultsCopper death is primarily caused by abnormal intracellular copper accumulation binding to acylated proteins in the tricarboxylic acid cycle, leading to protein oligomerization, downregulation of iron-sulfur cluster protein expression, triggering a toxic stress response, and ultimately cell death. The occurrence and progression of MAFLD are closely associated with genes associated with the copper death pathway. Imbalanced copper metabolism can lead to insulin resistance, causing abnormalities in blood glucose and lipid metabolism, promoting fat accumulation in the liver, and ultimately contributing to the development of MAFLD. Targeting genes involved in the copper death pathway can delay the progression of MAFLD. ConclusionThe occurrence and progression of MAFLD are closely linked to the copper death signaling pathway, with copper metabolism imbalance as a core component. This pathway not only directly leads to hepatocyte death but also triggers insulin resistance and abnormal lipid metabolism, jointly driving the progression of MAFLD. Therefore, targeted regulation of the copper death pathway is a novel therapeutic strategy to slow the progression of MAFLD.