Redox Imbalance and Mitochondrial Abnormalities in Kidney Disease
Yan, Liang-Jun
Redox Imbalance and Mitochondrial Abnormalities in Kidney Disease - Basel MDPI - Multidisciplinary Digital Publishing Institute 2022 - 1 electronic resource (200 p.)
Open Access
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.
Creative Commons
English
books978-3-0365-3758-0 9783036537573 9783036537580
10.3390/books978-3-0365-3758-0 doi
Medicine
Pharmacology
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 diabetes kidney mitochondria Oryza sativa rice husk TCA cycle metabolites kidney diseases renalase chronic kidney disease major adverse cardiovascular outcomes cadmium kidney injury renal toxicity oxidative damage proximal tubule controlled oxygenated rewarming mitochondrial uncoupling rewarming injury temperature paradox redox mitochondrial dysfunction SGLT2 mitochondrial reactive oxygen species Warburg effect podocytopathies mitochondrial oxidative stress reactive oxygen species (ROS) antioxidant defense cell death n/a
Redox Imbalance and Mitochondrial Abnormalities in Kidney Disease - Basel MDPI - Multidisciplinary Digital Publishing Institute 2022 - 1 electronic resource (200 p.)
Open Access
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.
Creative Commons
English
books978-3-0365-3758-0 9783036537573 9783036537580
10.3390/books978-3-0365-3758-0 doi
Medicine
Pharmacology
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 diabetes kidney mitochondria Oryza sativa rice husk TCA cycle metabolites kidney diseases renalase chronic kidney disease major adverse cardiovascular outcomes cadmium kidney injury renal toxicity oxidative damage proximal tubule controlled oxygenated rewarming mitochondrial uncoupling rewarming injury temperature paradox redox mitochondrial dysfunction SGLT2 mitochondrial reactive oxygen species Warburg effect podocytopathies mitochondrial oxidative stress reactive oxygen species (ROS) antioxidant defense cell death n/a