Redox Imbalance and Mitochondrial Abnormalities in Kidney Disease
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, hyperte...
Format: | eBook |
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Language: | English |
Published: |
Basel
MDPI - Multidisciplinary Digital Publishing Institute
2022
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Subjects: | |
Online Access: | Open Access: DOAB: description of the publication Open Access: DOAB, download the publication |
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072 | 7 | |a M |2 bicssc | |
072 | 7 | |a MKG |2 bicssc | |
720 | 1 | |a Yan, Liang-Jun |4 edt | |
720 | 1 | |a Yan, Liang-Jun |4 oth | |
245 | 0 | 0 | |a Redox Imbalance and Mitochondrial Abnormalities in Kidney Disease |
260 | |a Basel |b MDPI - Multidisciplinary Digital Publishing Institute |c 2022 | ||
300 | |a 1 online resource (200 p.) | ||
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520 | |a 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. | ||
540 | |a Creative Commons |f https://creativecommons.org/licenses/by/4.0/ |2 cc |u https://creativecommons.org/licenses/by/4.0/ | ||
546 | |a English | ||
650 | 7 | |a Medicine and Nursing |2 bicssc | |
650 | 7 | |a Pharmacology |2 bicssc | |
653 | |a acute kidney injury (AKI) | ||
653 | |a antioxidant defense | ||
653 | |a biogenesis | ||
653 | |a cadmium | ||
653 | |a caloric restriction | ||
653 | |a cell death | ||
653 | |a chronic kidney disease | ||
653 | |a chronic kidney disease (CKD) | ||
653 | |a controlled oxygenated rewarming | ||
653 | |a diabetes | ||
653 | |a diabetic kidney disease | ||
653 | |a fatty acid (FA) β-oxidation | ||
653 | |a ischemia | ||
653 | |a kidney | ||
653 | |a kidney allograft | ||
653 | |a kidney diseases | ||
653 | |a kidney injury | ||
653 | |a kidney rejection | ||
653 | |a major adverse cardiovascular outcomes | ||
653 | |a mitochondria | ||
653 | |a mitochondrial dynamics | ||
653 | |a mitochondrial dysfunction | ||
653 | |a mitochondrial homeostasis | ||
653 | |a mitochondrial metabolism | ||
653 | |a mitochondrial oxidative stress | ||
653 | |a mitochondrial proteins | ||
653 | |a mitochondrial reactive oxygen species | ||
653 | |a mitochondrial redox signaling | ||
653 | |a mitochondrial uncoupling | ||
653 | |a mitophagy | ||
653 | |a n/a | ||
653 | |a NADH/NAD+ | ||
653 | |a Oryza sativa | ||
653 | |a oxidative damage | ||
653 | |a oxidative phosphorylation (OXPHOS) | ||
653 | |a oxidative stress | ||
653 | |a podocytopathies | ||
653 | |a proximal tubule | ||
653 | |a reactive oxygen species (ROS) | ||
653 | |a redox | ||
653 | |a redox imbalance | ||
653 | |a renal toxicity | ||
653 | |a renalase | ||
653 | |a rewarming injury | ||
653 | |a rice husk | ||
653 | |a SGLT2 | ||
653 | |a TCA cycle metabolites | ||
653 | |a temperature paradox | ||
653 | |a tricarboxylic acid (TCA) cycle | ||
653 | |a Warburg effect | ||
793 | 0 | |a DOAB Library. | |
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856 | 4 | 0 | |u https://mdpi.com/books/pdfview/book/5361 |7 0 |z Open Access: DOAB, download the publication |