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dc.contributor.editorYan, Liang-Jun
dc.date.accessioned2022-05-06T11:22:07Z
dc.date.available2022-05-06T11:22:07Z
dc.date.issued2022
dc.identifierONIX_20220506_9783036537573_85
dc.identifier.urihttps://directory.doabooks.org/handle/20.500.12854/81019
dc.description.abstractThe 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.
dc.languageEnglish
dc.subject.classificationbic Book Industry Communication::M Medicine
dc.subject.classificationbic Book Industry Communication::M Medicine::MM Other branches of medicine::MMG Pharmacology
dc.subject.otherdiabetic kidney disease
dc.subject.othercaloric restriction
dc.subject.otherNADH/NAD+
dc.subject.otherredox imbalance
dc.subject.othermitochondrial homeostasis
dc.subject.othermitophagy
dc.subject.otheroxidative stress
dc.subject.otherkidney allograft
dc.subject.otherkidney rejection
dc.subject.otherischemia
dc.subject.otheracute kidney injury (AKI)
dc.subject.otherchronic kidney disease (CKD)
dc.subject.othertricarboxylic acid (TCA) cycle
dc.subject.othermitochondrial metabolism
dc.subject.othermitochondrial redox signaling
dc.subject.othermitochondrial proteins
dc.subject.otheroxidative phosphorylation (OXPHOS)
dc.subject.otherfatty acid (FA) β-oxidation
dc.subject.othermitochondrial dynamics
dc.subject.otherbiogenesis
dc.subject.otherdiabetes
dc.subject.otherkidney
dc.subject.othermitochondria
dc.subject.otherOryza sativa
dc.subject.otherrice husk
dc.subject.otherTCA cycle metabolites
dc.subject.otherkidney diseases
dc.subject.otherrenalase
dc.subject.otherchronic kidney disease
dc.subject.othermajor adverse cardiovascular outcomes
dc.subject.othercadmium
dc.subject.otherkidney injury
dc.subject.otherrenal toxicity
dc.subject.otheroxidative damage
dc.subject.otherproximal tubule
dc.subject.othercontrolled oxygenated rewarming
dc.subject.othermitochondrial uncoupling
dc.subject.otherrewarming injury
dc.subject.othertemperature paradox
dc.subject.otherredox
dc.subject.othermitochondrial dysfunction
dc.subject.otherSGLT2
dc.subject.othermitochondrial reactive oxygen species
dc.subject.otherWarburg effect
dc.subject.otherpodocytopathies
dc.subject.othermitochondrial oxidative stress
dc.subject.otherreactive oxygen species (ROS)
dc.subject.otherantioxidant defense
dc.subject.othercell death
dc.subject.othern/a
dc.titleRedox Imbalance and Mitochondrial Abnormalities in Kidney Disease
dc.typebook
oapen.identifier.doi10.3390/books978-3-0365-3758-0
oapen.relation.isPublishedBy46cabcaa-dd94-4bfe-87b4-55023c1b36d0
oapen.relation.isbn9783036537573
oapen.relation.isbn9783036537580
oapen.pages200
oapen.place.publicationBasel


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