LEADER 05197nam 2201537z- 450 001 9910585934503321 005 20231214133056.0 035 $a(CKB)5600000000483143 035 $a(oapen)https://directory.doabooks.org/handle/20.500.12854/91183 035 $a(EXLCZ)995600000000483143 100 $a20202208d2022 |y 0 101 0 $aeng 135 $aurmn|---annan 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 10$aImpaired Mitochondrial Bioenergetics under Pathological Conditions 210 $aBasel$cMDPI - Multidisciplinary Digital Publishing Institute$d2022 215 $a1 electronic resource (460 p.) 311 $a3-0365-4648-0 311 $a3-0365-4647-2 330 $aMitochondria 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. 606 $aResearch & information: general$2bicssc 606 $aBiology, life sciences$2bicssc 606 $aBiochemistry$2bicssc 610 $aaging heart 610 $aBcl-2 family 610 $amitochondria 610 $aprogrammed cell death 610 $afatty acid oxidation 610 $apalmitate 610 $aoleate 610 $am.3243A> 610 $aG mutation 610 $aMT-ATP6 610 $am.8909T> 610 $aC 610 $aATP synthase 610 $anephropathy 610 $aoxidative phosphorylation 610 $amitochondrial disease 610 $acardiolipin 610 $aBarth syndrome 610 $aSengers syndrome 610 $arespiratory chain 610 $aDilated Cardiomyopathy with Ataxia 610 $acardiomyopathy 610 $amammalian complex I 610 $aNADH dehydrogenase 610 $acomplex I assembly 610 $acomplex I structure 610 $acomplex I deficiency 610 $asupernumerary subunits 610 $aelectron transport chain 610 $amitochondrial dysfunction 610 $aLeigh syndrome 610 $amitochondrial diseases 610 $ayeast 610 $aSaccharomyces cerevisiae 610 $apet mutants 610 $apancreatic endocrine cells 610 $amathematical model 610 $acellular bioenergetics 610 $adiabetes 610 $aglucagon 610 $ainsulin 610 $aexercise 610 $aimmune system 610 $ametabolic disease 610 $aCOVID-19 610 $amitochondrial dynamics 610 $aviral infections 610 $aMAVS 610 $aRIG-I 610 $aMDA5 610 $ainnate immune response 610 $aSARS CoV-2 610 $aRSV 610 $ainfluenza 610 $arespiratory supercomplexes 610 $aROS 610 $aATP synthase/hydrolase 610 $amitochondrial permeability transition pore 610 $acristae 610 $acellular signaling 610 $ahuman disease 610 $amitochondrial dynamic 610 $acell signaling 610 $acancer 610 $arespiratory complexes 610 $aoxidative stress 610 $amitochondrial DNA 610 $aMTCYB mutations 610 $acytochrome b 610 $acomplex III 610 $aaging 610 $aenergy metabolism 610 $aentorhinal cortex 610 $alipoxidation-derived damage 610 $aneurodegeneration 610 $aoxidative damage 610 $aprotein import 610 $arespiratory complex assembly 610 $asupercomplexes 610 $amitochondrial proteostasis 610 $aheart failure 610 $abioenergetics 610 $aassembly factor 610 $aatypical myopathy 610 $ahigh-resolution respirometry 610 $atoxicity assays 610 $acell culture 610 $aequine primary myoblasts 610 $afibroblasts 610 $afrozen tissue 610 $aleukocytes 610 $aoxygen consumption 610 $aplatelets 610 $arespirometry 610 $askeletal muscle 615 7$aResearch & information: general 615 7$aBiology, life sciences 615 7$aBiochemistry 700 $aLenaz$b Giorgio$4edt$0100854 702 $aNesci$b Salvatore$4edt 702 $aLenaz$b Giorgio$4oth 702 $aNesci$b Salvatore$4oth 906 $aBOOK 912 $a9910585934503321 996 $aImpaired Mitochondrial Bioenergetics under Pathological Conditions$93035973 997 $aUNINA