01010cam0 2200289 450 E60020002886620210330113932.020070903d1959 |||||ita|0103 baitaITPotereGuglielmo Ferreroa cura di Gina Ferrero Lombrosointrtroduzione di Umberto Capagnolapostfazione di Leo Valiani2ed.MilanoEdizioni di Comunità1959387 p.22 cmFerrero, GuglielmoAF0001386907067954Valiani, LeoA600200039303070Lombroso Ferrero, GinaA600200043010070Campagnolo, UmbertoA600200043011070ITUNISOB20210330RICAUNISOBUNISOB90070765E600200028866M 102 Monografia moderna SBNM900002411Si70765acquistopregresso2UNISOBUNISOB20070903105839.020210330113854.0rovitoPouvoir37645UNISOB05234nam 2201561z- 450 991058593450332120220812(CKB)5600000000483143(oapen)https://directory.doabooks.org/handle/20.500.12854/91183(oapen)doab91183(EXLCZ)99560000000048314320202208d2022 |y 0engurmn|---annantxtrdacontentcrdamediacrrdacarrierImpaired Mitochondrial Bioenergetics under Pathological ConditionsBaselMDPI - Multidisciplinary Digital Publishing Institute20221 online resource (460 p.)3-0365-4648-0 3-0365-4647-2 Mitochondria are the powerhouses of cells; however, mitochondrial dysfunction causes energy depletion and cell death in a variety of diseases. Altered oxidative phosphorylation and ion homeostasis are associated with ROS production resulting from the disassembly of respiratory supercomplexes and the disruption of electron transfer chains. In pathological conditions, the dysregulation of mitochondrial homeostasis promotes Ca2+ overload in the matrix and ROS accumulation, which induces the mitochondrial permeability transition pore formation responsible for mitochondrial morphological changes linked to membrane dynamics, and ultimately, cell death. Finally, studies on the impaired mitochondrial bioenergetics in pathology could provide molecular tools to counteract diseases associated with mitochondrial dysfunction.BiochemistrybicsscBiology, life sciencesbicsscResearch & information: generalbicsscagingaging heartassembly factorATP synthaseATP synthase/hydrolaseatypical myopathyBarth syndromeBcl-2 familybioenergeticsCcancercardiolipincardiomyopathycell culturecell signalingcellular bioenergeticscellular signalingcomplex I assemblycomplex I deficiencycomplex I structurecomplex IIICOVID-19cristaecytochrome bdiabetesDilated Cardiomyopathy with Ataxiaelectron transport chainenergy metabolismentorhinal cortexequine primary myoblastsexercisefatty acid oxidationfibroblastsfrozen tissueG mutationglucagonheart failurehigh-resolution respirometryhuman diseaseimmune systeminfluenzainnate immune responseinsulinLeigh syndromeleukocyteslipoxidation-derived damagem.3243A&gtm.8909T&gtmammalian complex Imathematical modelMAVSMDA5metabolic diseasemitochondriamitochondrial diseasemitochondrial diseasesmitochondrial DNAmitochondrial dynamicmitochondrial dynamicsmitochondrial dysfunctionmitochondrial permeability transition poremitochondrial proteostasisMT-ATP6MTCYB mutationsn/aNADH dehydrogenasenephropathyneurodegenerationoleateoxidative damageoxidative phosphorylationoxidative stressoxygen consumptionpalmitatepancreatic endocrine cellspet mutantsplateletsprogrammed cell deathprotein importrespiratory chainrespiratory complex assemblyrespiratory complexesrespiratory supercomplexesrespirometryRIG-IROSRSVSaccharomyces cerevisiaeSARS CoV-2Sengers syndromeskeletal musclesupercomplexessupernumerary subunitstoxicity assaysviral infectionsyeastBiochemistryBiology, life sciencesResearch & information: generalLenaz Giorgioedt100854Nesci SalvatoreedtLenaz GiorgioothNesci SalvatoreothBOOK9910585934503321Impaired Mitochondrial Bioenergetics under Pathological Conditions3035973UNINA