Elsevier eBooks, Journal Year: 2024, Volume and Issue: unknown, P. 179 - 194
Published: Nov. 29, 2024
Language: Английский
Cell Death Discovery, Journal Year: 2025, Volume and Issue: 11(1)
Published: Jan. 24, 2025
Abstract Free radicals, characterized by the presence of unpaired electrons, are highly reactive species that play a significant role in human health. These molecules can be generated through various endogenous processes, such as mitochondrial respiration and immune cell activation, well exogenous sources, including radiation, pollution, smoking. While free radicals essential for certain physiological signaling defense, their overproduction disrupt delicate balance between oxidants antioxidants, leading to oxidative stress. Oxidative stress results damage critical biomolecules like DNA, proteins, lipids, contributing pathogenesis diseases. Chronic conditions cancer, cardiovascular diseases, neurodegenerative disorders, inflammatory diseases have been strongly associated with harmful effects radicals. This review provides comprehensive overview characteristics types mechanisms formation, biological impacts. Additionally, we explore natural compounds extracts studied antioxidant properties, offering potential therapeutic avenues managing radical-induced damage. Future research directions also discussed advance our understanding treatment radical-associated
Language: Английский
Citations
23
Neurobiology of Disease, Journal Year: 2023, Volume and Issue: 187, P. 106314 - 106314
Published: Oct. 1, 2023
Poly (ADP-ribose) polymerase-1 (PARP-1) is the most extensively studied member of PARP superfamily, with its primary function being facilitation DNA damage repair processes. Parthanatos a type regulated cell death cascade initiated by PARP-1 hyperactivation, which involves multiple subroutines, including accumulation ADP-ribose polymers (PAR), binding PAR and apoptosis-inducing factor (AIF), release AIF from mitochondria, translocation AIF/macrophage migration inhibitory (MIF) complex, massive MIF-mediated fragmentation. Over past few decades, role in central nervous system health disease has received increasing attention. In this review, we discuss biological functions neural proliferation differentiation, memory formation, brain ageing, epigenetic regulation. We then elaborate on involvement PARP-1-dependant parthanatos various neuropathological processes, such as oxidative stress, neuroinflammation, mitochondrial dysfunction, excitotoxicity, autophagy damage, endoplasmic reticulum (ER) stress. Additional highlight contains PARP-1's implications initiation, progression, therapeutic opportunities for different neurological illnesses, neurodegenerative diseases, stroke, autism spectrum disorder (ASD), sclerosis (MS), epilepsy, neuropathic pain (NP). Finally, emerging insights into repurposing inhibitors management diseases are provided. This review aims to summarize exciting advancements critical disorders, may open new avenues options targeting or parthanatos.
Language: Английский
Citations
29
International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(16), P. 12555 - 12555
Published: Aug. 8, 2023
This review explores the emerging role of hydrogen sulfide (H
Language: Английский
Citations
24
Journal of Integrated Science and Technology, Journal Year: 2025, Volume and Issue: 13(3)
Published: Jan. 7, 2025
The environmental pollution poses a serious global health risk, contributing to high morbidity and mortality rates. Neurological disorders, such as Alzheimer's, Parkinson's, Schizophrenia, ALS, Huntington's disease, are increasingly prevalent characterized by both structural functional abnormalities in neurons of the brain spinal cord. Understanding neuro-impact toxins is crucial for developing effective prevention intervention strategies. This review article investigates complex interactions between neurological health, focusing on their role development progression neurodegenerative neuropsychiatric disorders. Key mechanisms include oxidative stress, mitochondrial dysfunction, and, disruption neurotransmitter systems. It highlights pathways through which these exert effects, presents epidemiological evidence linking toxin exposure discusses potential public implications. By elucidating connections, paper aims enhance understanding determinants health.
Language: Английский
Citations
1
Archives of Pharmacal Research, Journal Year: 2024, Volume and Issue: 47(6), P. 571 - 595
Published: May 19, 2024
Language: Английский
Citations
9
Neurobiology of Disease, Journal Year: 2024, Volume and Issue: 201, P. 106663 - 106663
Published: Sept. 7, 2024
Language: Английский
Citations
7
CNS Neuroscience & Therapeutics, Journal Year: 2024, Volume and Issue: 30(10)
Published: Oct. 1, 2024
Huntington's disease (HD) is a devastating neurodegenerative that manifested by gradual loss of physical, cognitive, and mental abilities. As the advances, age has major impact on pathogenic signature mutant huntingtin (mHTT) protein aggregation. This review aims to explore intricate relationship between aging, mHTT toxicity, cellular senescence in HD. Scientific data interplay mHTT, HD were collected from several academic databases, including PubMed, Google Scholar, Google, ScienceDirect. The search terms employed "AGING," "HUNTINGTON'S DISEASE," "MUTANT HUNTINGTIN," "CELLULAR SENESCENCE." Additionally, gather information molecular mechanisms potential therapeutic targets, was extended include relevant such as "DNA DAMAGE," "OXIDATIVE STRESS," "AUTOPHAGY." According research, aging leads worsening pathophysiology through some processes. result accumulation, promoted, which causes DNA damage, oxidative stress, decreased autophagy, increased inflammatory responses. Pro-inflammatory cytokines other substances are released senescent cells, may worsen neuronal damage course disease. It been shown treatments directed at these pathways reduce symptoms enhance longevity experimental animals, pointing new possibility treating condition. Through their amplification harmful effects play crucial roles development Comprehending interplays creates novel opportunities for measures targeted alleviating enhancing patients' quality life.
Language: Английский
Citations
7
Neural Regeneration Research, Journal Year: 2023, Volume and Issue: 19(9), P. 1991 - 1997
Published: Dec. 14, 2023
Huntington's disease is a neurodegenerative caused by the expansion mutation of cytosine-adenine-guanine triplet in exon 1 HTT gene which responsible for production huntingtin (Htt) protein. In physiological conditions, Htt involved many cellular processes such as cell signaling, transcriptional regulation, energy metabolism DNA maintenance, axonal trafficking, and antiapoptotic activity. When genetic alteration present, mutant version (mHtt) occurs, characterized plethora pathogenic activities that, finally, lead to death. Among all cells mHtt exerts its dangerous activity, GABAergic Medium Spiny Neurons seem be most affected mHtt-induced excitotoxicity both cortex striatum. However, neurodegeneration proceeds ahead neuronal loss grows also other brain areas cerebellum, hypothalamus, thalamus, subthalamic nucleus, globus pallidus, substantia nigra, determining variety symptoms that characterize disease. From clinical point view, wide spectrum spanning from motor impairment cognitive disorders dementia. shows prevalence around 3.92 cases every 100,000 worldwide an incidence 0.48 new 100,000/year. To date, there no available cure Several treatments have been developed so far, aiming reduce severity one or more slow down inexorable decline this context, search reliable strategies target different aspects become utmost interest. recent years, studies demonstrated detrimental role condition highlighting how replacement lost would reasonable strategy overcome neurodegeneration. numerous attempts several preclinical models evaluate feasibility invasive non-invasive approaches. Thus, aim review offer overview appealing approaches stem cell-based therapy extracellular vesicles exosomes light promoting neurogenesis, discussing results obtained their limits future perspectives regarding neural regeneration context
Language: Английский
Citations
16
International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(23), P. 12767 - 12767
Published: Nov. 27, 2024
The tryptophan-kynurenine (KYN) pathway has long been recognized for its essential role in generating metabolites that influence various physiological processes. Traditionally, these have categorized into distinct, often opposing groups, such as pro-oxidant versus antioxidant, excitotoxic/neurotoxic neuroprotective. This dichotomous framework shaped much of the research on conditions like neurodegenerative and neuropsychiatric disorders, well cancer, where metabolic imbalances are a key feature. effects significantly influenced by factors, including concentration particular cellular milieu which they generated. A molecule acts neuroprotective at low concentrations may exhibit neurotoxic elevated levels. oxidative equilibrium surrounding environment can alter function KYN from an antioxidant to pro-oxidant. narrative review offers comprehensive examination analysis contemporary understanding metabolites, emphasizing their multifaceted biological functions relevance numerous pathological underscores pressing necessity paradigm shift comprehension metabolism. Understanding context-dependent roles is vital novel therapies Alzheimer's disease, multiple sclerosis, cancer. Comprehensive modulation, balancing inflammatory signals enzyme regulation, promising avenues targeted, effective treatments.
Language: Английский
Citations
5
Redox Biology, Journal Year: 2025, Volume and Issue: 81, P. 103537 - 103537
Published: Feb. 8, 2025
Reactive oxygen species (ROS) play a pivotal role in maintaining tissue homeostasis, yet their overabundance can impair normal cellular functions, induce cell death, and potentially lead to neurodegenerative disorders. This study identifies Drosophila Glycoprotein 93 (Gp93) as crucial factor that safeguards homeostasis preserves neuronal functions by preventing ROS-induced, JNK-dependent apoptotic death. Firstly, loss of Gp93 induces apoptosis primarily through the induction ROS. Secondary, neuro-specific depletion results ROS-JNK-mediated neurodegeneration. Thirdly, overexpression effectively curtails oxidative stress neurodegeneration caused paraquat exposure or aging process. Furthermore, these be substituted its human ortholog, HSP90B1. Lastly, HSP90B1 cultured cells triggers ROS production, JNK activation, apoptosis. Thus, this not only unveils novel physiological function Gp93, but also provides valuable insights for understanding pathological
Language: Английский
Citations
0