Redox Imbalance and Mitochondrial Abnormalities in Kidney Disease

Edited by
April 2022
200 pages
  • ISBN978-3-0365-3757-3 (Hardback)
  • ISBN978-3-0365-3758-0 (PDF)

This book is a reprint of the Special Issue Redox Imbalance and Mitochondrial Abnormalities in Kidney Disease that was published in

Biology & Life Sciences
Medicine & Pharmacology

The kidney performs important functions in the human body and can inflict either acute kidney injury (AKI) or chronic kidney disease (CKD). AKI can be induced by kidney ischemia, drugs such as cisplatin, and heavy metals such as cadmium and arsenic. CKD can be induced by drugs, heavy metals, hypertension, and diabetes, as well as cancer. Importantly, nearly all kidney disorders have been shown to involve redox imbalance, reductive stress, oxidative stress, and mitochondrial abnormalities such as impaired mitochondrial homeostasis, including disrupted mitophagy and deranged mitochondrial unfolded protein responses. Understanding how these redox-related dysregulated pathways operate may give us new insights into how to design novel approaches to fighting kidney disease. This Special Issue of Biomolecules entitled “Redox imbalance and mitochondrial abnormalities in kidney disease” covers a variety of topics focusing on oxidative stress, mitochondrial dysfunction, and antioxidation enhancement implicated in kidney disease or kidney transplantation.

  • Hardback
© 2022 by the authors; CC BY-NC-ND license
diabetic kidney disease; caloric restriction; NADH/NAD+; redox imbalance; mitochondrial homeostasis; mitophagy; oxidative stress; kidney allograft; kidney rejection; ischemia; acute kidney injury (AKI); chronic kidney disease (CKD); tricarboxylic acid (TCA) cycle; mitochondrial metabolism; mitochondrial redox signaling; mitochondrial proteins; oxidative phosphorylation (OXPHOS); fatty acid (FA) β-oxidation; mitochondrial dynamics; biogenesis; mitophagy; diabetes; kidney; mitochondria; Oryza sativa; oxidative stress; rice husk; mitochondria; TCA cycle metabolites; kidney diseases; renalase; chronic kidney disease; major adverse cardiovascular outcomes; cadmium; kidney injury; renal toxicity; mitochondria; oxidative damage; proximal tubule; controlled oxygenated rewarming; mitochondrial uncoupling; rewarming injury; temperature paradox; redox; diabetic kidney disease; oxidative stress; mitochondrial dysfunction; SGLT2; diabetic kidney disease; mitochondrial dysfunction; mitochondrial reactive oxygen species; Warburg effect; podocytopathies; mitochondrial oxidative stress; reactive oxygen species (ROS); antioxidant defense; cell death; n/a