Reprint

Impaired Mitochondrial Bioenergetics under Pathological Conditions

Edited by
July 2022
460 pages
  • ISBN978-3-0365-4648-3 (Hardback)
  • ISBN978-3-0365-4647-6 (PDF)

This book is a reprint of the Special Issue Impaired Mitochondrial Bioenergetics under Pathological Conditions that was published in

Biology & Life Sciences
Medicine & Pharmacology
Public Health & Healthcare
Summary

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.

Format
  • Hardback
License
© by the authors
Keywords
aging heart; Bcl-2 family; mitochondria; programmed cell death; fatty acid oxidation; palmitate; oleate; m.3243A> G mutation; MT-ATP6; m.8909T> C; ATP synthase; nephropathy; oxidative phosphorylation; mitochondrial disease; cardiolipin; mitochondria; Barth syndrome; Sengers syndrome; respiratory chain; Dilated Cardiomyopathy with Ataxia; cardiomyopathy; mitochondria; mammalian complex I; NADH dehydrogenase; complex I assembly; complex I structure; complex I deficiency; supernumerary subunits; electron transport chain; mitochondrial dysfunction; Leigh syndrome; mitochondrial diseases; respiratory chain; yeast; Saccharomyces cerevisiae; pet mutants; pancreatic endocrine cells; mathematical model; mitochondrial dysfunction; cellular bioenergetics; diabetes; glucagon; insulin; exercise; mitochondria; immune system; metabolic disease; COVID-19; mitochondria; mitochondrial dynamics; viral infections; MAVS; RIG-I; MDA5; innate immune response; SARS CoV-2; RSV; influenza; oxidative phosphorylation; respiratory supercomplexes; ROS; ATP synthase/hydrolase; mitochondrial dysfunction; mitochondrial permeability transition pore; cristae; cellular signaling; ATP synthase; human disease; mitochondria; mitochondrial dynamic; cell signaling; ROS; cancer; respiratory complexes; respiratory supercomplexes; oxidative stress; mitochondrial DNA; MTCYB mutations; cytochrome b; complex III; mitochondrial diseases; aging; ATP synthase; energy metabolism; entorhinal cortex; lipoxidation-derived damage; mitochondrial dysfunction; neurodegeneration; oxidative damage; protein import; mitochondrial dysfunction; respiratory complex assembly; supercomplexes; neurodegeneration; mitochondrial proteostasis; mitochondria; heart failure; bioenergetics; mitochondrial dynamics; mitochondrial disease; Leigh syndrome; NADH dehydrogenase; respiratory chain; oxidative phosphorylation; assembly factor; atypical myopathy; high-resolution respirometry; toxicity assays; cell culture; equine primary myoblasts; bioenergetics; fibroblasts; frozen tissue; leukocytes; mitochondria; oxygen consumption; platelets; respirometry; skeletal muscle; n/a