4.7 Editorial Material

Redox Imbalance and Mitochondrial Abnormalities in Kidney Disease

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Summary: The reduction-oxidation (redox) system involves the coordination of different electron gradients produced by enzymatic reactions. These reactions generate reactive oxygen species (ROS) and reactive nitrogen species (RNS), which play important roles in cell signaling pathways and cellular processes. However, excessive production of these oxidants can lead to oxidative stress (OS), which is pathological. OS is a major contributor to the onset of diabetic kidney disease (DKD). In DKD, glucose-induced toxicity promotes OS and mitochondrial dysfunction, impairing the function of proximal tubular cells in the kidney. Increased glucose levels and ROS enhance the activity of sodium/glucose co-transporter type 2 (SGLT2), further exacerbating OS. SGLT2 inhibitors have shown cardiovascular benefits in DKD, possibly by promoting a balanced equilibrium between oxidant and antioxidant mechanisms.

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NADH/NAD+ Redox Imbalance and Diabetic Kidney Disease

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Folic acid-induced animal model of kidney disease

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Summary: The kidneys are vulnerable to both acute kidney injury (AKI) and chronic kidney disease (CKD), with animal models being crucial for studying the pathological mechanisms of kidney disease. This article reviews a widely used animal model of kidney disease induced by folic acid (FA), discussing the major mechanisms of FA-induced kidney injury and its application in testing therapeutic approaches.

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