Loliolide combats glutamate-induced neurotoxicity by oxidative stress through MAPK/Nrf2 pathway in hippocampal neuronal cells DOI
Hyun‐Soo Kim, Jayeon Cheon, Kirinde Gedara Isuru Sandanuwan Kirindage

et al.

Algal Research, Journal Year: 2024, Volume and Issue: unknown, P. 103866 - 103866

Published: Dec. 1, 2024

Language: Английский

Oxidative Stress and Bio-Regulation DOI Open Access

Toshikazu Yoshikawa,

Fukka You

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(6), P. 3360 - 3360

Published: March 15, 2024

Reactive oxygen species (ROS) and free radicals work to maintain homeostasis in the body, but their excessive production causes damage organism. The human body is composed of a variety cells totaling over 60 trillion cells. Each cell performs different functions has unique lifespan. lifespan preprogrammed genes, death that have reached end called apoptosis. This contrary necrosis, which premature brought about by physical or scientific forces. its own lifespan, humans estimated be up 120 years. Elucidating mechanism single will lead better understanding death, and, conversely, exploring mechanisms life. In this sense, research on active radicals, are implicated biological disorders homeostasis, requires an both physicochemical as well biochemical aspects. Based discussion above, it clear see dual injuring facilitating living organisms.

Language: Английский

Citations

27

Mitochondrial DNA leakage: underlying mechanisms and therapeutic implications in neurological disorders DOI Creative Commons
Guangming Zhang,

Huayuan Wei,

Anliu Zhao

et al.

Journal of Neuroinflammation, Journal Year: 2025, Volume and Issue: 22(1)

Published: Feb. 7, 2025

Mitochondrial dysfunction is a pivotal instigator of neuroinflammation, with mitochondrial DNA (mtDNA) leakage as critical intermediary. This review delineates the intricate pathways leading to mtDNA release, which include membrane permeabilization, vesicular trafficking, disruption homeostatic regulation, and abnormalities in dynamics. The escaped activates cytosolic sensors, especially cyclic gmp-amp synthase (cGAS) signalling inflammasome, initiating neuroinflammatory cascades via pathways, exacerbating spectrum neurological pathologies. therapeutic promise targeting discussed detail, underscoring necessity for multifaceted strategy that encompasses preservation homeostasis, prevention leakage, reestablishment dynamics, inhibition activation sensors. Advancing our understanding complex interplay between neuroinflammation imperative developing precision interventions disorders.

Language: Английский

Citations

3

Interplay among Oxidative Stress, Autophagy, and the Endocannabinoid System in Neurodegenerative Diseases: Role of the Nrf2- p62/SQSTM1 Pathway and Nutraceutical Activation DOI Creative Commons
Federica Armeli, Beatrice Mengoni, Debra L. Laskin

et al.

Current Issues in Molecular Biology, Journal Year: 2024, Volume and Issue: 46(7), P. 6868 - 6884

Published: July 2, 2024

The onset of neurodegenerative diseases involves a complex interplay pathological mechanisms, including protein aggregation, oxidative stress, and impaired autophagy. This review focuses on the intricate connection between stress autophagy in disorders, highlighting as pivotal disease pathogenesis. Reactive oxygen species (ROS) play dual roles cellular homeostasis regulation, with disruptions redox signaling contributing to neurodegeneration. activation Nrf2 pathway represents critical antioxidant mechanism, while maintains by degrading altered cell components. interaction among p62/SQSTM1, Nrf2, Keap1 forms regulatory essential for response, whose dysregulation leads aggregate accumulation. Targeting Nrf2-p62/SQSTM1 holds promise therapeutic intervention, mitigating preserving functions. Additionally, this explores potential synergy endocannabinoid system neuroprotection. Further research is needed elucidate involved molecular mechanisms develop effective strategies against

Language: Английский

Citations

10

Oxidative Metabolism in Brain Ischemia and Preconditioning: Two Sides of the Same Coin DOI Creative Commons

Elena D’Apolito,

Maria Josè Sisalli, Michele Tufano

et al.

Antioxidants, Journal Year: 2024, Volume and Issue: 13(5), P. 547 - 547

Published: April 29, 2024

Brain ischemia is one of the major causes chronic disability and death worldwide. It related to insufficient blood supply cerebral tissue, which induces irreversible or reversible intracellular effects depending on time intensity ischemic event. Indeed, neuronal function may be restored in some conditions, such as transient attack (TIA), responsible for protecting against a subsequent lethal insult. well known that brain requires high levels oxygen glucose ensure cellular metabolism energy production damage caused by impairment tightly brain’s low antioxidant capacity. Oxygen key player mitochondrial oxidative phosphorylation (OXPHOS), during reactive species (ROS) synthesis can occur physiological side-product process. besides producing adenosine triphosphate (ATP) under normal mitochondria are primary source ROS within cell. This because, 0.2–2% cases, escape electrons from complex I (NADPH-dehydrogenase) III electron transport chain occurring ATP leads superoxide radical anion (O2•−), exerts detrimental owing its molecular instability. Along with ROS, nitrosative (RNS) also contribute free radicals. When accumulation RNS occurs, it cause membrane lipid peroxidation DNA damage. Here, we describe pathways activated tissue after lethal/sub event like stroke tolerance, respectively, highlighting important role played stress dysfunction onset two different conditions.

Language: Английский

Citations

9

Mitochondrial DNA Leakage and cGas/STING Pathway in Microglia: Crosstalk Between Neuroinflammation and Neurodegeneration DOI
Yuqian Liu,

Bohan Zhang,

Ruonan Duan

et al.

Neuroscience, Journal Year: 2024, Volume and Issue: 548, P. 1 - 8

Published: April 27, 2024

Language: Английский

Citations

7

Pterostilbene nanoemulsion promotes Nrf2 signaling pathway to downregulate oxidative stress for treating Alzheimer’s disease DOI
Jingyu Liu,

Jikai Xu,

Luan Jia

et al.

International Journal of Pharmaceutics, Journal Year: 2024, Volume and Issue: 655, P. 124002 - 124002

Published: March 16, 2024

Language: Английский

Citations

5

The function of previously unappreciated exerkines secreted by muscle in regulation of neurodegenerative diseases DOI Creative Commons
Xuepeng Bian, Qian Wang, Yibing Wang

et al.

Frontiers in Molecular Neuroscience, Journal Year: 2024, Volume and Issue: 16

Published: Jan. 5, 2024

The initiation and progression of neurodegenerative diseases (NDs), distinguished by compromised nervous system integrity, profoundly disrupt the quality life patients, concurrently exerting a considerable strain on both economy social healthcare infrastructure. Exercise has demonstrated its potential as an effective preventive intervention rehabilitation approach among emerging therapeutics targeting NDs. As largest secretory organ, skeletal muscle possesses capacity to secrete myokines, these myokines can partially improve prognosis NDs mediating muscle-brain axis. Besides well-studied exerkines, which are secreted during exercise that pivotally exert their beneficial function, physiological function novel e.g., apelin, kynurenic acid (KYNA), lactate have been underappreciated previously. Herein, this review discusses roles exerkines mechanisms in regulating improvement NDs, especially significance functions improving NDs’ prognoses through exercise. Furthermore, several with implications ameliorating ND proposed future direction for investigation. Elucidation regulation advances understanding pathogenesis facilitates development intervene processes cure

Language: Английский

Citations

4

Chronic Sleep Deprivation Impairs Visual Functions via Oxidative Damage in Mice DOI Creative Commons
Liying Tang,

Houjian Zhang,

Yi Liao

et al.

American Journal Of Pathology, Journal Year: 2024, Volume and Issue: 194(2), P. 307 - 320

Published: Jan. 21, 2024

Language: Английский

Citations

4

Development and validation of a prognostic prediction model for elderly gastric cancer patients based on oxidative stress biochemical markers DOI Creative Commons
Xingqi Zhang,

Ze-Ning Huang,

Wu Ju

et al.

BMC Cancer, Journal Year: 2025, Volume and Issue: 25(1)

Published: Feb. 1, 2025

The potential of the application artificial intelligence and biochemical markers oxidative stress to predict prognosis older patients with gastric cancer (GC) remains unclear. This retrospective multicenter study included consecutive GC aged ≥ 65 years treated between January 2012 April 2018. were allocated into three cohorts (training, internal, external validation). GC-Integrated Oxidative Stress Score (GIOSS) was developed using Cox regression correlate patient prognosis. Predictive models for five-year overall survival (OS) constructed random forest (RF), decision tree (DT), support vector machine (SVM) methods, validated area under curve (AUC) calibration plots. SHapley Additive exPlanations (SHAP) method used model interpretation. a total 1,859 patients. results demonstrated that low GIOSS predictor poor RF most efficient method, AUCs 0.999, 0.869, 0.796 in training, internal validation, validation sets, respectively. DT SVM showed AUC values. Calibration analyses considerable clinical usefulness model. SHAP identified pN, pT, perineural invasion, tumor size, as key predictive features. An online web calculator based on best Incorporating GIOSS, effectively predicts postoperative OS is robust prognostic tool. Our findings emphasize importance provide pathway improved management GC. Retrospectively registered at ClinicalTrials.gov (trial registration number: NCT06208046, date registration: 2024–05-01).

Language: Английский

Citations

0

Blood DNA Methylation in Nuclear and Mitochondrial Sequences Links to Malnutrition and Poor Prognosis in ALS: A Longitudinal Study DOI Open Access
Antía Fernández‐Pombo, Andrea G. Izquierdo,

Ana Cantón-Blanco

et al.

Nutrients, Journal Year: 2025, Volume and Issue: 17(8), P. 1295 - 1295

Published: April 8, 2025

Background: Malnutrition in amyotrophic lateral sclerosis (ALS) is associated with disease severity, and epigenetic regulation may be involved. The aim of this study was to assess the methylation levels specific DNA sequences from nuclear mitochondrial genomes a population ALS elucidate their relationship nutritional status evolution disease. Methods: Patients were evaluated between 2013 2021 (n = 66). They categorized according status, using Global Leadership Initiative on (GLIM) criteria, progression, Functional Rating (ALSFRS-R) Scale. samples extracted leukocytes at time diagnosis for analysis markers oxidative stress, function global (D-loop, GSTP1, LINE-1). Results: According GLIM 29 (43.9%) patients had malnutrition (22.7%—moderate; 21.2%—severe), which positively correlated progression (r 0.414; p < 0.01) death 0.687; 0.01). Mortality occurred 43.9% (median death, 18.7 (1.7–82.7) months). A significant association observed D-loop, CpG1 site LINE-1 malnutrition, diagnosis, death. D-loop best predictor (AUC, 0.79; 0.01), 0.70; mortality 0.71; Conclusions: This revealed, first time, early detection as potential biomarker ALS, useful personalized management aimed counteracting progression.

Language: Английский

Citations

0