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2+) and Their Signaling in Alzheimer's and Other Neurological-Related Disorders
Published in Suvardhan Kanchi, Rajasekhar Chokkareddy, Mashallah Rezakazemi, Smart Nanodevices for Point-of-Care Applications, 2022
Neha Chauhan, Smita Jain, Kanika Verma, Swapnil Sharma, Raghuraj Chouhan, Veera Sadhu
In contrast, it is already a known fact that an overload of mitochondrial Ca2+ can result in cell apoptosis [3]. Redundant Ca2+ uptake disrupts the proton gradient between IMM on both sides, which results in bio-energetic impairment and apoptosis of cells due to necrosis. Although, [Ca2+]mito also has the ability to activate cell apoptosis in finer ways, stimulating cells to apoptotic stimuli [23]. Especially, the physiological oscillations in mitochondria [Ca2+] do not induce mitochondria PTP opening per [Ca2+]mito level elevates favoring the opening of PTP by binding itself toward cyclophilin-D, resulting in inducing pro-apoptotic factorial discharge in the cytosol (like cytochrome-c) and activating apoptotic-cascade. However, some observation has been made that VDAC1 selectively transmits apoptotic Ca2+ signaling to mitochondria, assembling a mediation via Grp75 with IP3Rs (especially IP3R-3) [18, 22]. This mediation is a not static one but tends to improve with apoptotic-stimuli. Moreover, Fis-1 (mitochondrial-fission-protein) has been showcased to transmit apoptotic signaling from mitochondria to the ER, through communication with Bap31 at the ER. Hence, it assists pro-apoptotic p20Bap31 cleavage, an incident correlated with Ca2+ discharge from ER and mitochondrial activation for apoptosis [24].
Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
MFN proteins are the best characterized fusion regulators, whereas mitochondrial fission protein 1 (FIS1) and dynamin-related protein 1 (DRP1) control fission.913 MFN1 and MFN2 are dynamin-related GTPases expressed on the OMM that tether mitochondria together during fusion, although MFNB2 is also expressed on MAMs and regulates mitochondrial-ER tethering.915
Computation of the mitochondrial age distribution along the axon length
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2022
Ivan A. Kuznetsov, Andrey V. Kuznetsov
Renewal of mitochondrial proteins involves mitochondrial fusion and fission (Misgeld and Schwarz 2017). Fusion of old and new mitochondria leads to an exchange of old and new soluble and membrane-bound components, such as mitochondrial proteins (Malka et al. 2005; Patel et al. 2013). It is believed that mitochondrial fission leads to the separation of mutated copies of the mitochondrial genome into a separate mitochondrion, which is then recycled by the autophagosome (Twig et al. 2008; Safiulina and Kaasik 2013). Fission also serves as a mechanism that prevents mitochondria from becoming excessively long, so longer mitochondria are more likely to enter fission than shorter ones (Cagalinec et al. 2013). If fission events are unopposed, they can lead to complete fragmentation of the mitochondrial network (Ahola et al. 2019). Mitochondrial fusion accelerates mitochondrial fission, which is necessary to maintain a constant average length of mitochondria. Fission is important for autophagy, the mechanism of mitochondria removal (Twig et al. 2008).
Epigenetic modifications associated with pathophysiological effects of lead exposure
Published in Journal of Environmental Science and Health, Part C, 2019
Madiha Khalid, Mohammad Abdollahi
Pb-induced apoptosis has also been observed with chromosomal condensation, cell body shrinkage, and marginalization.81,289,290 Altered expression of mitochondrial fission and fusion protein are linked to apoptosis.80,291 Toxic metals are known to alter liver enzymes such as ATPases.96,277 Histological and electron microscopic analysis of rat hippocampus revealed a significant number of dead and dying apoptotic cells due to 500 ppm Pb exposure characterized by increased ratio value of Bax/Bcl-2 (P < 0.01). Pb-exposed cells displayed an irregular nuclear membrane, clumped chromatin, presence of nuclear fragments and apoptotic bodies.292 Similarly, long-term 500 ppm Pb exposure was reported to cause overexpression of poly ADP-ribose polymerase (PARP), caspase-3 and Bcl-2 protein in adult rat brain.293 Moreover, Pb-induced apoptosis is also linked to histone hyperacetylation in cardiovascular tissues of rats upon 1% Pb exposure, along with Bax upregulation with Bcl-2 downregulation.70 In another study, increased apoptotic effects in rat cerebella granule cells were caused by 10 μM Pb, with cell shrinkage and chromatin condensation.294 Human mesangial cells (HMCs) upon 5, 10, or 20 μmol/L Pb treatment demonstrated apoptosis and nuclear fragmentation due to Pb-induced oxidative stress via triggering malondialdehyde (MDA) and lactate dehydrogenase (LDH) activity.295 All this evidence suggests the potential role of Pb in inducing apoptosis via dysregulating energy metabolism and oxidative stress.