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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
The best understood mitochondrial functions include ATP production by oxidative phosphorylation, β-oxidation of fatty acids, and metabolism of amino acids and lipids. (11). Mitochondria also have other complex functions, including participating in a variety of cell-signaling cascades. Proteins such as GTPases, kinases, and phosphatases facilitate bidirectional communication between the mitochondria and the rest of the cell, helping to regulate metabolism, cell cycle control, development, and antiviral responses (12). A key example of the mitochondria's integration in signaling pathways is its role in the apoptotic cascade (13), with mitochondrial fragmentation and cristae remodeling being essential steps for cytochrome c release and cell death (12). Additionally, calcium signaling causes a dynamic change in the phosphorylation state of numerous proteins (14). Mitochondria act both as a calcium buffer and as the propagator of intracellular calcium waves during muscle contraction and synaptic vesicle release (12). Another example of the integration of mitochondria in signaling pathways is its role in the apoptotic cascade and cell death (13); indeed, mitochondrial fragmentation and cristae remodeling are essential steps for “cytochrome c” release and cell death (12).
Role of Vitamin D and Antioxidants in the Prevention and Treatment of Alzheimer’s Disease
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Shilia Jacob Kurian, Ruby Benson, Sonal Sekhar Miraj, Mahadev Rao
Dysregulation in intracellular calcium signaling is widely implicated in the pathophysiology of AD, which results in lesions, hyperphosphorylation of tau, and finally neurodegeneration. Mitochondrial activities largely depend on calcium from the endoplasmic reticulum (ER) or extracellular space. Inositol 1,4,5-trisphosphate (IP3) is the second messenger and the inositol 1,4,5-trisphosphate receptors (IP3Rs) are intracellular ion channels, which stimulate the release of calcium from the ER (Bizzarri et al. 2016; Egorova and Bezprozvanny 2018).
Exploration of Nanonutraceuticals in Neurodegenerative Diseases
Published in Raj K. Keservani, Anil K. Sharma, Rajesh K. Kesharwani, Nutraceuticals and Dietary Supplements, 2020
Swati Pund, Amita Joshi, Vandana Patravale
The hallmarks of neurodegenerative diseases are the elevated levels of malondialdehyde as well as protein carbonyl levels, which are the outcomes of reduced mitochondrial membrane potential, and disruption of intracellular calcium signaling due to increased oxidative stress (Chowdhury et al., 2016; Domijan et al., 2014; Turillazzi et al., 2016). Oxidative stress generates reactive oxygen species (ROS) via, two main cellular organelles, namely, mitrochondria and plasma membrane. The by-product of cellular metabolism generated in mitrochondria is ROS. In mitrochondria, unpaired electrons that escape the electron transport chain react with molecular oxygen to generate superoxide radicals. While, in plasma membrane reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity results in ROS generation (Sadhukhan et al., 2018). A minimum amount of ROS is essential for normal human physiology; however, accumulation of ROS is toxic. Basal ROS homeostasis in body is maintained via various delicate balances between ROS scavengers like dietary antioxidants, glutathione, NADPH, and so forth, and ROS inducers like hypoxia, stress, metabolic defects, and so forth. Failure of this delicate redox balance leads to “oxidative stress” resulting in damaging effects seen as aging, diabetes, cognitive impairment, and neurodegenerative disorders like, AD, PD, ALS, HD (Mao et al., 2018).
Effects of potassium channel knockdown on peripheral blood T lymphocytes and NFAT signaling pathway in Xinjiang Kazak patients with hypertension
Published in Clinical and Experimental Hypertension, 2023
Chen Dai, Meng Tan, Xiaopan Meng, Jian Dong, Yuanming Zhang
Previous studies have demonstrated that the potassium channels and nuclear factor of activated T cells (NFAT) are closely related to the T lymphocyte activation (17,18). There are two major types of membrane ion channels on T lymphocytes, namely the voltage-gated potassium channels (Kv1.3) and calcium-activated potassium channels (KCa3.1) (19). These channels help maintain membrane potential by mediating the outflow of potassium, while the altered membrane potential would indirectly affect the calcium signaling within the cells (20). Therefore, the potassium channels on T lymphocytes are closely related to the intracellular Ca2+ regulation. Calcium is an important second messenger associated with the NFAT signaling pathway. Increased Ca2+ concentration can activate the calcineurin (CaN), which triggers the T lymphocyte activation through NFAT signaling pathway (21) 1. The NFAT signaling pathway can also mediate the lymphocyte proliferation and differentiation. Furthermore, NFAT would activate the production of cytokines, including the tumor necrosis factor-α, IL-4, IL-6, and IFN-β (22). Whether the potassium channels are involved in the occurrence of inflammatory state in the body through the NFAT signaling pathway remains to be elucidated.
Calcium Intake Contributed by Whole Foods and Gastric Cancer in Viet Nam: A Case‑Control Study
Published in Nutrition and Cancer, 2023
Thinh Gia Nguyen, Dung Thuy Thi Truong, Phuoc Hong Le, Tuyen Cat Kim Vo, Shunya Ikeda, Ngoan Tran Le
Calcium is vital to human life as it maintains skeletal and tissue architecture and plays important roles in coagulation and the control of cell behavior (8). Calcium signaling in these pathways is crucial for the development of cancer. Ca2+ channels and pumps are potential therapeutic targets for cancer treatment (9). This suggests that dietary calcium intake can, to some extent, affect cancer cells. Evidence implies that calcium intake is associated with colorectal, lung, prostate, and breast cancer incidence (10). However, only a few studies have assessed the association between calcium intake and GC. We found only one cohort study by the National Institutes of Health-American Association of Retired Persons (NIH-AARP) reporting this association (11). Nevertheless, the previous study did not assess the serum status of H. pylori infection as a significant risk factor for GC (5). Therefore, we aimed to explore the relationship between calcium intake and GC in the Vietnamese population after controlling for confounding variables, including H. pylori infection.
Toxoplasma gondii infection and risk of attention-deficit hyperactivity disorder: a systematic review and meta-analysis
Published in Pathogens and Global Health, 2020
Tooran Nayeri, Shahabeddin Sarvi, Mahmood Moosazadeh, Zahra Hosseininejad, Afsaneh Amouei, Ahmad Daryani
T. gondii affects the expression of approximately 3000 host genes throughout its life cycle. Susceptibility genes for mental disorders, such as ADHD, are highly enriched in the human arm of this interactome. Moreover, the expression of 17.7% of 237 ADHD susceptibility genes is affected by the Toxoplasma infection [55,56]. Furthermore, the primary common emphasis in ADHD was on the calcium-signaling pathway and number of other metabolic pathways, such as tyrosine, tryptophan, and histidine, and the number of recovered genes in this pathway is 44 [55,57]. The calcium-signaling pathway is activated by voltage or receptor-gated ion channels, processes modulating intracellular stores, and phosphatidylinositol signaling system [58]. Calcium channel blockers, calmodulin antagonism, or extracellular calcium reduce cell invasion by parasites [59,60].