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Infiltration of Macrophages and Oxidative stress in IgA Nephropathy

Cheng Liu*

Diabetic nephropathy (DN) is the second most frequent and prevalent consequence of diabetes mellitus (DM). A chronic hyperglycemic state that can cause oxidative damage to macromolecules (lipids, carbohydrates, proteins, and nucleic acids) is what causes an increase in the generation of oxidative stress (OS). The expression of the DNA repairer enzyme is influenced by OS, which promotes the creation of oxidative damage to the histones of the double-chain DNA, which results in apoptosis, the cell death process. The presence of inflammation, growth, and an increase in the synthesis of the extracellular matrix (ECM) in DN are all caused by the chronic hyperglycemic state’s release of an increase in advanced glycation end-products (AGE), which interact through cellular receptors to favour activation of the transcription factor NF-B and the protein kinase C (PKC) system. Due to the fact that prolonged hyperglycemia enhances ROS generation, ROS play a significant role in the pathophysiology of diabetes complications. The mitochondria, which have the ability to produce more endogenous antioxidants than necessary, are the main cause of the excessive generation of ROS. There are several approaches to particular treatment targets or adjuvant management options in the control of glycaemia in DN