Redox Dysregulation and Mitochondrial Adaptation in Kidney Disease

Dear Colleagues,

The kidneys perform important functions in our body and can experience either acute kidney injury (AKI) or chronic kidney disease (CKD). AKI can be induced by renal ischemia–reperfusion injury, by drugs such as cisplatin, and by heavy metals such as cadmium and arsenic. CKD can be induced by drugs, heavy metals, hypertension, diabetes, and cancer. Importantly, nearly all kidney disorders have been shown to involve redox dysregulation or redox imbalance that initially begins with NADH reductive stress and then transitions to oxidative stress. This pathological process usually involves mitochondrial adaptation and mitochondrial abnormalities such as mitochondrial stress response, impaired mitochondrial homeostasis, disrupted mitophagy, and disturbed mitochondrial unfolded protein response. Understanding how these redox-related dysregulated pathways leading to kidney disorders may give us novel insights into how to design innovative approaches to fighting kidney disease.

This Special Issue will cover all topics related to AKI and CKD and will especially welcome submissions of manuscripts on redox mechanisms and the pathophysiology underlying AKI, CKD, and diabetic nephropathy or diabetic kidney disease (DKD). It should be noted that this Special Issue will consider the publication of both review articles and original research articles.

Dr. Liang-Jun Yan
Guest Editor

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