01176nam2 2200265 i 450 SUN004406520090202120000.020060411d1979 |0itac50 baitaIT|||| |||||ˆ1: ‰TextJames H. StubblebinePrincetonPrinceton universityc1979XI, 226 p., [1] c. di tav.29 cm.001SUN00440642001 Duccio di Buoninsegna and his schoolJames H. Stubblebine1210 PrincetonPrinceton university215 v.29 cm.USPrincetonSUNL000078Stubblebine, James H.SUNV035589215538Princeton universitySUNV000300650Stubblebine, J. H.Stubblebine, James H.SUNV065577ITSOL20181109RICASUN0044065UFFICIO DI BIBLIOTECA DEL DIPARTIMENTO DI LETTERE E BENI CULTURALI07 CONS Pa Duccio 2183/1 07 15638 UFFICIO DI BIBLIOTECA DEL DIPARTIMENTO DI LETTERE E BENI CULTURALIIT-CE010315638CONS Pa Duccio 2183/1caText1404028UNICAMPANIA03901nam 2200937z- 450 991056646570332120231214133250.0(CKB)5680000000037723(oapen)https://directory.doabooks.org/handle/20.500.12854/81019(EXLCZ)99568000000003772320202205d2022 |y 0engurmn|---annantxtrdacontentcrdamediacrrdacarrierRedox Imbalance and Mitochondrial Abnormalities in Kidney DiseaseBaselMDPI - Multidisciplinary Digital Publishing Institute20221 electronic resource (200 p.)3-0365-3757-0 3-0365-3758-9 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.MedicinebicsscPharmacologybicsscdiabetic kidney diseasecaloric restrictionNADH/NAD+redox imbalancemitochondrial homeostasismitophagyoxidative stresskidney allograftkidney rejectionischemiaacute kidney injury (AKI)chronic kidney disease (CKD)tricarboxylic acid (TCA) cyclemitochondrial metabolismmitochondrial redox signalingmitochondrial proteinsoxidative phosphorylation (OXPHOS)fatty acid (FA) β-oxidationmitochondrial dynamicsbiogenesisdiabeteskidneymitochondriaOryza sativarice huskTCA cycle metaboliteskidney diseasesrenalasechronic kidney diseasemajor adverse cardiovascular outcomescadmiumkidney injuryrenal toxicityoxidative damageproximal tubulecontrolled oxygenated rewarmingmitochondrial uncouplingrewarming injurytemperature paradoxredoxmitochondrial dysfunctionSGLT2mitochondrial reactive oxygen speciesWarburg effectpodocytopathiesmitochondrial oxidative stressreactive oxygen species (ROS)antioxidant defensecell deathMedicinePharmacologyYan Liang-Junedt1314102Yan Liang-JunothBOOK9910566465703321Redox Imbalance and Mitochondrial Abnormalities in Kidney Disease3031708UNINA