Journal of Hazardous Materials, Journal Year: 2024, Volume and Issue: 471, P. 134297 - 134297
Published: April 12, 2024
Language: Английский
Journal of Hazardous Materials, Journal Year: 2024, Volume and Issue: 471, P. 134297 - 134297
Published: April 12, 2024
Language: Английский
Physiological Reviews, Journal Year: 2023, Volume and Issue: 103(4), P. 2349 - 2422
Published: April 6, 2023
Mitochondria are well known as organelles responsible for the maintenance of cellular bioenergetics through production ATP. Although oxidative phosphorylation may be their most important function, mitochondria also integral synthesis metabolic precursors, calcium regulation, reactive oxygen species, immune signaling, and apoptosis. Considering breadth responsibilities, fundamental metabolism homeostasis. Appreciating this significance, translational medicine has begun to investigate how mitochondrial dysfunction can represent a harbinger disease. In review, we provide detailed overview metabolism, bioenergetics, dynamics, autophagy, damage-associated molecular patterns, mitochondria-mediated cell death pathways, at any these levels is associated with disease pathogenesis. Mitochondria-dependent pathways thereby an attractive therapeutic target ameliorating human
Language: Английский
Citations
281ACS Chemical Neuroscience, Journal Year: 2023, Volume and Issue: 14(17), P. 2944 - 2954
Published: Aug. 10, 2023
Alzheimer's disease (AD) is an insidious and progressive neurodegenerative disorder that affects millions of people worldwide. Although the pathogenesis remains obscure, there are two dominant causal hypotheses. Since last three decades, amyloid beta (Aβ) deposition was most prominent hypothesis, other tau hyperphosphorylation hypothesis. The confirmed diagnostic criterion for AD presence neurofibrillary tangles (NFTs) composed hyperphosphorylated toxic oligomeric Aβ in autopsied brain. Consistent with these hypotheses, oxidative stress (OS) garnering major attention research. OS results from imbalance pro-oxidants antioxidants. There a considerable debate scientific community on which process occurs first, or plaque deposition/tau hyperphosphorylation. Based recent observations various laboratories including ours along critical analysis those information, we believe early event leads to as well dimerization protein its subsequent This hypothesis immediately suggests consideration novel therapeutic approaches include antioxidants involving glutathione enrichment brain by supplementation without iron chelator.
Language: Английский
Citations
75Antioxidants, Journal Year: 2025, Volume and Issue: 14(1), P. 108 - 108
Published: Jan. 18, 2025
The study of mitochondrial dysfunction has become increasingly pivotal in elucidating the pathophysiology various cerebral pathologies, particularly neurodegenerative disorders. Mitochondria are essential for cellular energy metabolism, regulation reactive oxygen species (ROS), calcium homeostasis, and execution apoptotic processes. Disruptions function, driven by factors such as oxidative stress, excitotoxicity, altered ion balance, lead to neuronal death contribute cognitive impairments several brain diseases. Mitochondrial can arise from genetic mutations, ischemic events, hypoxia, other environmental factors. This article highlights critical role progression diseases discusses need targeted therapeutic strategies attenuate damage, restore enhance neuroprotection.
Language: Английский
Citations
2Life Sciences, Journal Year: 2023, Volume and Issue: 319, P. 121432 - 121432
Published: Jan. 25, 2023
Language: Английский
Citations
35Biomaterials, Journal Year: 2023, Volume and Issue: 301, P. 122284 - 122284
Published: Aug. 17, 2023
Language: Английский
Citations
33Cellular Signalling, Journal Year: 2023, Volume and Issue: 109, P. 110794 - 110794
Published: July 6, 2023
Traditionally, mitochondria are known as "the powerhouse of the cell," responsible for energy (ATP) generation (by electron transport chain, oxidative phosphorylation, tricarboxylic acid cycle, and fatty ß-oxidation), regulation several metabolic processes, including redox homeostasis, calcium signalling, cellular apoptosis. The extensive studies conducted in last decades portray multifaceted signalling organelles that ultimately command cells' survival or death. Based on current knowledge, we'll outline mitochondrial to other intracellular compartments homeostasis pathology-related stress conditions here. following topics discussed: (i) mtROS mitohormesis, (ii) Ca2+ signalling; (iii) anterograde (nucleus-to-mitochondria) retrograde (mitochondria-to-nucleus) signal transduction, (iv) mtDNA role immunity inflammation, (v) induction mitophagy- apoptosis - cascades, (vi) dysfunctions (mitochondriopathies) cardiovascular, neurodegenerative, malignant diseases. novel insights into molecular mechanisms mitochondria-mediated can explain adaptation environmental stresses achieve cell survival.
Language: Английский
Citations
30APOPTOSIS, Journal Year: 2023, Volume and Issue: 29(3-4), P. 482 - 502
Published: Nov. 30, 2023
Language: Английский
Citations
30The Neuroscientist, Journal Year: 2023, Volume and Issue: 30(4), P. 440 - 457
Published: Jan. 3, 2023
Alzheimer’s disease (AD) is characterized by the accumulation of amyloid β and phosphorylated τ protein aggregates in brain, which leads to loss neurons. Under microscope, function mitochondria uniquely primed play a pivotal role neuronal cell survival, energy metabolism, death. Research studies indicate that mitochondrial dysfunction, excessive oxidative damage, defective mitophagy neurons are early indicators AD. This review article summarizes latest development AD: 1) mechanism pathways, 2) importance functions, 3) metabolic pathways 4) link between dysfunction mechanisms AD, 5) potential mitochondrial-targeted therapeutics interventions treat patients with
Language: Английский
Citations
29Journal of the American Academy of Dermatology, Journal Year: 2024, Volume and Issue: 91(5), P. 793 - 802
Published: Feb. 2, 2024
Language: Английский
Citations
14Metabolism, Journal Year: 2024, Volume and Issue: 155, P. 155912 - 155912
Published: April 11, 2024
Language: Английский
Citations
11