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Mitochondrial outer membrane permeabilization (MOMP), also known as the mitochondrial outer membrane permeability, is one of two ways apoptosis (a type of programmed cell death) can be activated. [1] It is part of the intrinsic pathway of apoptosis, also known as the mitochondrial pathway. MOMP is known as the point of no return in apoptosis.
The mitochondrial permeability transition pore (mPTP or MPTP; also referred to as PTP, mTP or MTP) is a protein that is formed in the inner membrane of the mitochondria under certain pathological conditions such as traumatic brain injury and stroke.
PPIF is a major component of the mitochondrial permeability transition pore (MPTP) and, thus, highly involved in mitochondrial metabolism and apoptosis, as well as in mitochondrial diseases and related conditions, including cardiac diseases, neurodegenerative diseases, and muscular dystrophy. [7]
MOMP is the process before apoptosis, which is accompanied to permeability of the inner membrane of the mitochondria (IMM). Permeability transition pore (PTP) opening induces mitochondrial swelling and outer membrane of the mitochondria (OMM) rupture. Moreover, PTP opening induce releasing of caspase-activating factors and apoptosis.
Apart from exchange of ADP and ATP across the inner mitochondrial membrane, the ANT also exhibits an intrinsic uncoupling activity [1] [17] ANT is an important modulatory [18] and possible structural component of the Mitochondrial Permeability Transition Pore, a channel involved in various pathologies whose function still remains elusive. Karch ...
Like many of the Bcl-2 family proteins, BNIP3 modulates the permeability state of the outer mitochondrial membrane by forming homo- and hetero-oligomers inside the membrane. [6] Upregulation results in a decrease in mitochondrial potential, an increase in reactive oxygen species, mitochondrial swelling and fission, and an increase in ...
Examples of mitochondrial transport proteins include the following: The mitochondrial permeability transition pore, which opens in response to increased mitochondrial calcium (Ca 2+) load and oxidative stress [45] The mitochondrial calcium uniporter which transports calcium from the cytosol of the cell into the mitochondrial matrix [45] [46]
VDAC1's function in calcium ion transport has also been linked to neurodegenerative diseases. In PD, VDAC1 increases calcium ion levels within the mitochondria, resulting in increased mitochondrial permeability, disrupted mitochondrial membrane potential, elevated ROS production, cell death, and neuronal degeneration. [12]