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Neuromuscular Physiology
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
Inner membrane. The inner membrane is freely permeable only to oxygen, carbon dioxide, and water (5). About 60–70 % of the proteins in the mitochondria are found in the inner membrane, many of which are transport proteins, largely controlling the movement of various substances into and out of the matrix. The cristae extend into the matrix at different depths are the main sites of mitochondrial energy conversion. A small proton gradient between the intermembrane space (pH 7.2–7.4) and the matrix (pH 7.9–8) drives ATP production catalyzed by the ATP synthase enzymes in the membranes of the cristae.
Mitochondria and Embryo Viability
Published in Carlos Simón, Carmen Rubio, Handbook of Genetic Diagnostic Technologies in Reproductive Medicine, 2022
Irene Corachan Garcia, Laura Iñiguez Quiles, Antonio Diez-Juan
Mitochondria play a critical role in the generation of metabolic energy in eukaryotic cells, using oxidative phosphorylation to derive energy (ATP) from carbohydrates and fatty acids. Mitochondria contain their own DNA, which encodes tRNAs, rRNAs, and some mitochondrial proteins (1). Ranging in size from 0.5 to 1.0 μm in diameter (2), these unique organelles have a double-membrane system consisting of inner and outer membranes separated by an intermembrane space (1). The outer mitochondrial membrane encloses the matrix (internal space) and contains a large number of proteins that form channels allowing small molecules to pass. The inner mitochondrial membrane, which is folded into structures (cristae) that increase the surface area, is less permeable, blocking the movement of ions and other small molecules. Both the inner and outer membranes contain specific transport proteins that can move molecules by a passive or active transport (2) (Figure 15.1).
Mitochondria in Huntington’s Disease
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Mitochondria, OXPHOS, and HD: Mitochondria play a crucial role in generating and delivering cellular energy currency, that is, ATP. Mitochondria have an outer mitochondrial membrane (OMM) and an inner mitochondrial membrane (IMM), which has a larger surface area and is folded to fit inside OMM creating cristae. Cristae are the seat of mitochondrial oxidative phosphorylation (OXPHOS) machinery, namely, electron transport chain (ETC) complexes I–IV, two electron carriers, and a specialized ATP synthesizing enzyme called ATP synthase. The space between the two membranes of mitochondria is called intermembrane space and the space constrained by the IMM is called matrix, which is filled with a gel-like substance. The matrix contains the mtDNA and the enzymes of the tricarboxylic acid (TCA) cycle (also known as the citric acid cycle or Krebs cycle). Due to the high energy demand and limited regenerative capability of neurons, mitochondrial dysfunction (broadly including individual enzyme complex deficiencies or fusion-fission abnormalities or disrupted movement along the cytoskeletal elements) is especially debilitating for these specialized cells.
13-Acetoxysarcocrassolide induces apoptosis in human hepatocellular carcinoma cells through mitochondrial dysfunction and suppression of the PI3K/AKT/mTOR/p70S6K signalling pathway
Published in Pharmaceutical Biology, 2022
Chang-Min Hsu, Jen-Jie Lin, Jui-Hsin Su, Chih-I Liu
Studies have reported that apoptosis can occur through intrinsic and/or extrinsic pathways (Wajant 2002; Denicourt and Dowdy 2004; Matthews et al. 2012). The intrinsic pathway of apoptosis is also known as the mitochondria-mediated apoptotic pathway. Mitochondria-mediated apoptosis is regulated by the Bcl-2 family of proteins, where the balance between the pro-apoptotic protein Bax and the anti-apoptotic protein Bcl-2, the release of cytochrome c into the cytoplasm, and the activation of downstream caspases are all important factors responsible for triggering apoptosis (Putcha et al. 2002; Wang et al. 2006; Shankar and Srivastava 2007). The mitochondria-mediated apoptotic pathway is mainly caused by the movement of Bax, a proapoptotic protein of the Bcl-2 family, from the cytoplasm to the mitochondria after cell stimulation; it is binding to Bak, located in the outer mitochondrial membrane, to form a dimer; and its polymerization in the outer mitochondrial membrane to form a pore (Graham and Chen 2001; Broughton et al. 2009; Akpan and Troy 2013). After the formation of pores, apoptotic factors such as cytochrome c, apoptosis-inducing factor (AIF), and endonuclease G are released from the mitochondrial intermembrane space. Consequently, when cytochrome c is released into the cytoplasm, it binds to apoptotic protease activating factor-1 (Apaf-1), forming an apoptosome with pro-caspase 9, which then activates caspase 9. Next, caspase 3 is activated due to cleavage by caspase 9, which subsequently results in the cleavage of PARP-1, triggering apoptosis (Germain et al. 1999; Graham and Chen 2001; Broughton et al. 2009).
Sericin-mediated improvement of dysmorphic cardiac mitochondria from hypercholesterolaemia is associated with maintaining mitochondrial dynamics, energy production, and mitochondrial structure
Published in Pharmaceutical Biology, 2022
Kitiya Rujimongkon, Sumate Ampawong, Duangnate Isarangkul, Onrapak Reamtong, Pornanong Aramwit
High serum cholesterol is one of the factors that leads to myocardial and cardiac mitochondrial degeneration (Ampawong et al. 2017a). Ultrastructural observations of mitochondria have revealed four mitochondrial stages from a normal to a severely degenerated structure. The normal stage involves a structure containing double membranes (inner and outer membranes) covering the intermembrane space. The inner membrane forms pore-like structures termed crista junctions in the mitochondrial matrix. The swelling stage involves the first dysmorphic structure, which includes an increased size, distensions of the intercellular matrix, and partial disappearance of cristae. The spheroid stage is characterised by the complete loss of cristae and the formation of multiple cysts in the matrix. In the final stage, the ghost stage, the membrane disappears, leaving granular and electrodense material (Mariappan et al. 2007; Ampawong et al. 2017a, 2017b). Dysmorphic cardiac mitochondria under hypercholesterolemic coupled with hyperglycaemic conditions have revealed different numbers of mitochondria between the dysmorphic and normal stages (Ampawong et al. 2017a). This evidence suggests the possibility that high serum cholesterol levels are related to the structure of cardiac mitochondria, are associated with mitochondrial dysfunction and result in organ failure, especially in the heart.
Mitochondria as a key player in systemic lupus erythematosus
Published in Autoimmunity, 2022
Diana C. Quintero-González, Marcela Muñoz-Urbano, G. Vásquez
Mitochondria are organelles derived from an alpha-proteobacterium [12]; they are present in every cell of the human body, except for red blood cells, which show anaerobic metabolism. Mitochondria have four functional compartments (from the inside to the outside), including the matrix (MM), where DNA is harbored and metabolic reactions occur; the inner membrane (IM), which is characterized by respiratory chain proteins and a vast surface area owing to folding into multiple cristae; the intermembrane space, which is comparable to the cytosol; and the outer membrane (OM), which contains the voltage-dependent anion channel (VDAC) [13]. Furthermore, these organelles have developed several functions during their evolution, including adenosine triphosphate (ATP) production, lipid beta-oxidation, mtDNA transcription, mitochondrial reactive oxygen species (mROS) generation, apoptosis, maintenance of lipid membrane integrity, and calcium homeostasis [12]. Some mitochondrial functions are described below to improve our understanding of their relationship with SLE pathogenesis.