International Immunopharmacology, Год журнала: 2024, Номер 142, С. 113176 - 113176
Опубликована: Сен. 20, 2024
Язык: Английский
International Immunopharmacology, Год журнала: 2024, Номер 142, С. 113176 - 113176
Опубликована: Сен. 20, 2024
Язык: Английский
Frontiers in Pharmacology, Год журнала: 2024, Номер 15
Опубликована: Май 30, 2024
Traditionally, pharmacological mammalian/mechanistic targets of rapamycin (mTOR) kinase inhibitors have been used during transplantation and tumor treatment. Emerging pre-clinical evidence from the last decade displayed surprising effectiveness mTOR in ameliorating Alzheimer's Disease (AD), a common neurodegenerative disorder characterized by progressive cognitive function decline memory loss. Research shows activation as an early event AD development, inhibiting may promote resolution many hallmarks Alzheimer's. Aberrant protein aggregation, including amyloid-beta (Aβ) deposition tau filaments, defects, are reversed upon inhibition. A closer inspection highlighted temporal dependence hallmark-specific nature such beneficial effects. Time administration relative to disease progression, maintenance functional lysosomal system, could modulate its effectiveness. Moreover, inhibition also exerts distinct effects between neurons, glial cells, endothelial cells. Different properties produce different based on blood-brain barrier (BBB) entry capacities sites. This questions viable intervention strategy. In this review, we first summarize available their characteristics. We then comprehensively update discuss results resolve AD. Key pathologies discussed include Aβ deposition, tauopathies, aberrant neuroinflammation, neurovascular system breakdowns.
Язык: Английский
Процитировано
5Experimental Eye Research, Год журнала: 2025, Номер 251, С. 110235 - 110235
Опубликована: Янв. 9, 2025
Язык: Английский
Процитировано
0Frontiers in Cellular Neuroscience, Год журнала: 2025, Номер 19
Опубликована: Апрель 7, 2025
Neuroinflammation is a fundamental feature of many chronic neurodegenerative diseases, where it contributes to disease onset, progression, and severity. This persistent inflammatory state arises from the activation innate adaptive immune responses within central nervous system (CNS), orchestrated by complex interplay resident cells, infiltrating peripheral an array molecular mediators such as cytokines, chemokines, extracellular vesicles. Among CNS-resident microglia play role, exhibiting dynamic spectrum phenotypes ranging neuroprotective neurotoxic. In sustained microglial often leads amplification cascades, reinforcing pathogenic cycle immune-mediated damage. Intercellular communication inflamed CNS persistence progression neuroinflammation. Microglia engage in extensive crosstalk with astrocytes, neurons, oligodendrocytes, shaping both local systemic responses. These interactions influence key processes synaptic pruning, phagocytosis, blood-brain barrier integrity, cytokine-mediated signaling. Understanding mechanisms cell-cell signaling this context critical for identifying therapeutic strategies modulate response restore homeostasis. review explores players neuroinflammation, focus on role microglia, pathways underlying intercellular communication, potential approaches mitigate neuroinflammatory damage diseases.
Язык: Английский
Процитировано
0European Journal of Pharmacology, Год журнала: 2025, Номер 990, С. 177269 - 177269
Опубликована: Янв. 11, 2025
Язык: Английский
Процитировано
0Aquaculture, Год журнала: 2023, Номер 575, С. 739758 - 739758
Опубликована: Июнь 13, 2023
Язык: Английский
Процитировано
8Journal of Nanobiotechnology, Год журнала: 2024, Номер 22(1)
Опубликована: Ноя. 7, 2024
Abstract Optic nerve regeneration remains challenging worldwide due to the limited intrinsic regenerative capacity of retinal ganglion cells (RGCs) and inhibitory microenvironment. Oxidative stress, induced by excessive reactive oxygen species (ROS) following optic injury, is associated with prolonged neuroinflammation, resulting in a secondary injury RGCs impairment axon regeneration. Herein, we developed bionic nanocomposite scaffold (GA@PDA) immunoregulatory ability for enhanced The ice-templating method was employed fabricate biopolymer-based scaffolds directional porous structure, mimicking nerve, which effectively guided oriented growth neuronal cells. incorporation bioinspired polydopamine nanoparticles (PDA NPs) further confers excellent ROS scavenging ability, thereby modulating phenotype transformation microglia/macrophages from pro-inflammatory M1 anti-inflammatory M2. In rat crush model, implantation GA@PDA survival promoted axonal Our study offers novel insights holds promising potential advancement engineered biomaterials facilitating
Язык: Английский
Процитировано
2Neuropharmacology, Год журнала: 2023, Номер 242, С. 109746 - 109746
Опубликована: Окт. 12, 2023
Язык: Английский
Процитировано
5Molecular Aspects of Medicine, Год журнала: 2023, Номер 94, С. 101219 - 101219
Опубликована: Окт. 13, 2023
Язык: Английский
Процитировано
5Cell Proliferation, Год журнала: 2024, Номер 57(12)
Опубликована: Июль 18, 2024
Traumatic optic neuropathy refers to nerve (ON) injury by trauma, including explosion and traffic accident. Retinal ganglion cell (RGC) death is the critical pathological cause of irreversible visual impairment blindness in ON injury. We previously investigated patterns 11 modes mouse retina post-ON Here we aimed identify additional signalling pathways regulating RGC survival rodents RNA sequencing analysis identified upregulation inflammation cellular senescence-related genes injury, which were confirmed immunoblotting immunofluorescence analyses. Increased expression senescence-associated β-galactosidase (SA-βgal) RGCs activation microglia also found. Transforming growth factor-β receptor type II inhibitor (LY2109761) treatment suppressed p15
Язык: Английский
Процитировано
1Free Radical Biology and Medicine, Год журнала: 2023, Номер 212, С. 415 - 432
Опубликована: Дек. 20, 2023
Язык: Английский
Процитировано
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