Search results
Results From The WOW.Com Content Network
Mitochondrial respirometry measures the consumption of oxygen by the mitochondria without involving an entire living animal and is the main tool to study mitochondrial function. [13] Three different types of samples may be subjected to such respirometric studies: isolated mitochondria (from cell cultures, animals or plants); permeabilized cells ...
Mitochondrial biogenesis is the process by which cells increase mitochondrial numbers. [ 1 ] [ 2 ] It was first described by John Holloszy in the 1960s, when it was discovered that physical endurance training induced higher mitochondrial content levels, leading to greater glucose uptake by muscles. [ 3 ]
Formation of ROS as a mitochondrial waste product will eventually lead to cytotoxicity and cell death. Because of their role in metabolism, mitochondria are very susceptible to ROS damage. Damaged mitochondria cause a depletion in ATP and a release of cytochrome c, which leads to activation of caspases and onset of apoptosis. Mitochondrial ...
PGC-1α provides a direct link between external physiological stimuli and the regulation of mitochondrial biogenesis, and is a major factor causing slow-twitch rather than fast-twitch muscle fiber types. [10] Endurance exercise has been shown to activate the PGC-1α gene in human skeletal muscle. [11]
Midzone division is linked to mitochondrial biogenesis, which occurs when the cell is proliferating and requires an increased number of mitochondria. In contrast, peripheral division is associated with the removal of damaged mitochondrial units from the network, with these mitochondria being targeted for autophagy or mitophagy, leading to their ...
Cytochrome c is widely believed to be localised solely in the mitochondrial intermembrane space under normal physiological conditions. [27] The release of cytochrome c from mitochondria to the cytosol, where it activates the caspase family of proteases, is believed to be the primary trigger leading to the onset of apoptosis. [28]
Respiratory complex I, EC 7.1.1.2 (also known as NADH:ubiquinone oxidoreductase, Type I NADH dehydrogenase and mitochondrial complex I) is the first large protein complex of the respiratory chains of many organisms from bacteria to humans.
Most mutations of mitochondrial membrane transporters are autosomal recessive. Mutations to transporters within the inner mitochondrial membrane mostly affect high-energy tissues due to the disruption of oxidative phosphorylation. [4] [44] For example, decreased mitochondrial function has been linked to heart failure and hypertrophy. This ...