Extracellular vesicles: biological mechanisms and emerging therapeutic opportunities in neurodegenerative diseases DOI Creative Commons
Ling Wang, Xiaoyan Zhang,

Ziyi Yang

et al.

Translational Neurodegeneration, Journal Year: 2024, Volume and Issue: 13(1)

Published: Dec. 6, 2024

Abstract Extracellular vesicles (EVs) are membrane originating from different cells within the brain. The pathophysiological role of EVs in neurodegenerative diseases is progressively acknowledged. This field has advanced basic biological research to essential clinical significance. capacity selectively enrich specific subsets biofluids via distinctive surface markers opened new avenues for molecular understandings across various tissues and organs, notably In recent years, brain-derived have been extensively investigated as biomarkers, therapeutic targets, drug-delivery vehicles diseases. review provides a brief overview characteristics physiological functions classes EVs, focusing on mechanisms by which types mediate occurrence development Concurrently, novel approaches challenges use delivery delineated.

Language: Английский

Crosstalk Among Glial Cells in the Blood–Brain Barrier Injury After Ischemic Stroke DOI

Weizhuo Lu,

Jiyue Wen

Molecular Neurobiology, Journal Year: 2024, Volume and Issue: 61(9), P. 6161 - 6174

Published: Jan. 27, 2024

Language: Английский

Citations

11
Tackling the glial scar in spinal cord regeneration: new discoveries and future directions DOI Creative Commons
Areez Shafqat, Ibrahem Albalkhi, Hamzah M Magableh

et al.

Frontiers in Cellular Neuroscience, Journal Year: 2023, Volume and Issue: 17

Published: May 24, 2023

Axonal regeneration and functional recovery are poor after spinal cord injury (SCI), typified by the formation of an scar. While this scar was traditionally believed to be primarily responsible for axonal failure, current knowledge takes a more holistic approach that considers intrinsic growth capacity axons. Targeting SCI has also not reproducibly yielded nearly same efficacy in animal models compared these neuron-directed approaches. These results suggest major reason behind central nervous system (CNS) failure is but stimulate axon adequately. findings raise questions about whether targeting neuroinflammation glial scarring still constitute viable translational avenues. We provide comprehensive review dual role how future research can produce therapeutic strategies hurdles posed processes without compromising neuroprotection.

Language: Английский

Citations

22
Mesenchymal Stem Cell Therapy in Traumatic Spinal Cord Injury: A Systematic Review DOI Open Access
Rodrigo Montoto-Meijide, Rosa Meijide-Faílde, Silvia Díaz‐Prado

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(14), P. 11719 - 11719

Published: July 20, 2023

Recovery from a traumatic spinal cord injury (TSCI) is challenging due to the limited regenerative capacity of central nervous system restore cells, myelin, and neural connections. Cell therapy, particularly with mesenchymal stem cells (MSCs), holds significant promise for TSCI treatment. This systematic review aims analyze efficacy, safety, therapeutic potential MSC-based cell therapies in TSCI. A comprehensive search PUBMED COCHRANE databases until February 2023 was conducted, combining terms such as “spinal injury,” “stem cells,” therapy,” “mesenchymal “traumatic injury”. Among 53 studies initially identified, 22 (21 clinical trials 1 case series) were included. Findings these consistently demonstrate improvements AIS (ASIA Impairment Scale) grades, sensory scores, and, lesser extent, motor scores. Meta-analyses further support positive outcomes. have shown short- medium-term indicated by absence adverse events within studied timeframe. However, caution required when drawing generalized recommendations scientific evidence available. Further research needed elucidate long-term safety implications advancements. Although progress has been made, therapies, additional exploring other future gene neurostimulation techniques, tissue engineering approaches are essential understanding evolving treatment landscape.

Language: Английский

Citations

20
Tetramethylpyrazine alleviates ferroptosis and promotes functional recovery in spinal cord injury by regulating GPX4/ACSL4 DOI
Gang Liu, Bowen Deng,

Luyao Huo

et al.

European Journal of Pharmacology, Journal Year: 2024, Volume and Issue: 977, P. 176710 - 176710

Published: June 4, 2024

Language: Английский

Citations

8
Neuroinflammation and major depressive disorder: astrocytes at the crossroads DOI Creative Commons

Melissa Puentes-Orozco,

Sonia Luz Albarracín, María Marcela Velásquez Toledo

et al.

Frontiers in Cellular Neuroscience, Journal Year: 2024, Volume and Issue: 18

Published: Nov. 22, 2024

Major depressive disorder is a complex and multifactorial condition, increasingly linked to neuroinflammation astrocytic dysfunction. Astrocytes, along with other glial cells, beyond their classic functions in maintaining brain homeostasis, play crucial role regulating neuroplasticity, key processes the pathophysiology of depression. This mini-review explores involvement astrocytes depression emphasizing mediation processes, impact dysfunction on effect some antidepressants astrocyte reactivity. Recent evidence suggests that targeting astrocyte-related signaling pathways, particularly balance between different phenotypes, could offer promising for therapeutic strategies affective disorders. Therefore, deeper understanding biology may open way innovative treatments aimed at mitigating symptoms by impacting both imbalances neuroplasticity.

Language: Английский

Citations

6
A2 reactive astrocyte‐derived exosomes alleviate cerebral ischemia–reperfusion injury by delivering miR‐628 DOI Creative Commons

Ying-Ju Wang,

He‐Ping Li,

Hanwen Sun

et al.

Journal of Cellular and Molecular Medicine, Journal Year: 2024, Volume and Issue: 28(16)

Published: Aug. 1, 2024

Abstract Ischemia and hypoxia activate astrocytes into reactive types A1 A2, which play roles in damage protection, respectively. However, the function mechanism of A2 astrocyte exosomes are unknown. After were injected lateral ventricle, infarct volume, to blood–brain barrier (BBB), apoptosis expression microglia‐related proteins measured. The dual luciferase reporter assay was used detect target genes miR‐628, overexpressing A2‐Exos overexpressed knocked down miR‐628 constructed. qRT–PCR, western blotting immunofluorescence staining subsequently performed. obviously reduced BBB promoted M2 microglial polarization. RT–PCR showed that highly expressed A2‐Exos. Dual assays revealed NLRP3, S1PR3 IRF5 miR‐628. or down, protective effects increased decreased, pyroptosis polarization through inhibition via delivery This study explored action provided new therapeutic targets concepts for treating cerebral ischemia.

Language: Английский

Citations

5
The role of astrocyte in neuroinflammation in traumatic brain injury DOI Creative Commons
Liang He, Ruqiang Zhang,

Maiqiao Yang

et al.

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Journal Year: 2023, Volume and Issue: 1870(3), P. 166992 - 166992

Published: Dec. 19, 2023

Language: Английский

Citations

13
TL1A promotes the postoperative cognitive dysfunction in mice through NLRP3‐mediated A1 differentiation of astrocytes DOI Creative Commons
Genghuan Wang, Jian Shen, Liping Zhai

et al.

CNS Neuroscience & Therapeutics, Journal Year: 2023, Volume and Issue: 29(11), P. 3588 - 3597

Published: June 2, 2023

We investigated the mechanism, whereby tumor necrosis factor-like ligand 1A (TL1A) mediates A1 differentiation of astrocytes in postoperative cognitive dysfunction (POCD).The and behavioral abilities mice were assessed by Morris water maze open field tests, while levels key A2 astrocyte factors detected RT-qPCR. Immunohistochemical (IHC) staining was used to examine expression GFAP, western blot assay related proteins, enzyme-linked immunosorbent (ELISA) detect inflammatory cytokines.The results showed that TL1A could promote progression mice. Astrocytes differentiated into phenotype, unobvious changes noted biomarkers. Knockout NLRP3 or intervention with inhibitor inhibit effect TL1A, improving suppressing differentiation.Our demonstrate plays an important role POCD mice, which promotes through NLRP3, thereby exacerbating dysfunction.

Language: Английский

Citations

12
Management of the Brain: Essential Oils as Promising Neuroinflammation Modulator in Neurodegenerative Diseases DOI Creative Commons
Rosanna Avola,

Alessandro Giuseppe Furnari,

Adriana Carol Eleonora Graziano

et al.

Antioxidants, Journal Year: 2024, Volume and Issue: 13(2), P. 178 - 178

Published: Jan. 31, 2024

Neuroinflammation, a pivotal factor in the pathogenesis of various brain disorders, including neurodegenerative diseases, has become focal point for therapeutic exploration. This review highlights neuroinflammatory mechanisms that hallmark diseases and potential benefits essential oils counteracting neuroinflammation oxidative stress, thereby offering novel strategy managing mitigating impact disorders. Essential oils, derived from aromatic plants, have emerged as versatile compounds with myriad health benefits. exhibit robust antioxidant activity, serving scavengers free radicals contributing to cellular defense against stress. Furthermore, showcase anti-inflammatory properties, modulating immune responses inflammatory processes implicated chronic diseases. The intricate by which phytomolecules exert their effects were explored, shedding light on multifaceted properties. Notably, we discussed ability modulate diverse pathways crucial maintaining homeostasis suppressing responses, capacity rescue cognitive deficits observed preclinical models neurotoxicity

Language: Английский

Citations

4
Ruxolitinib improves the inflammatory microenvironment, restores glutamate homeostasis, and promotes functional recovery after spinal cord injury DOI Creative Commons
Jiang Cao,

Xiao Yu,

Jingcheng Liu

et al.

Neural Regeneration Research, Journal Year: 2024, Volume and Issue: 19(11), P. 2499 - 2512

Published: Jan. 31, 2024

JOURNAL/nrgr/04.03/01300535-202411000-00030/figure1/v/2024-04-10T160327Z/r/image-tiff The inflammatory microenvironment and neurotoxicity can hinder neuronal regeneration functional recovery after spinal cord injury. Ruxolitinib, a JAK-STAT inhibitor, exhibits effectiveness in autoimmune diseases, arthritis, managing cytokine storms. Although studies have shown the neuroprotective potential of ruxolitinib neurological trauma, exact mechanism by which it enhances injury, particularly its effect on astrocytes, remains unclear. To address this gap, we established mouse model T10 contusion found that effectively improved hindlimb motor function reduced area Transcriptome sequencing analysis showed alleviated inflammation immune response restored EAAT2 expression, glutamate levels, excitatory toxicity. Furthermore, inhibited phosphorylation JAK2 STAT3 injured decreased level nuclear factor kappa-B expression factors interleukin-1β, interleukin-6, tumor necrosis factor-α. Additionally, glutamate-induced excitotoxicity increased uptake inhibiting activation STAT3, thereby reducing neurotoxicity, calcium influx, oxidative stress, cell apoptosis, increasing complexity dendritic branching. Collectively, these results indicate restores homeostasis rescuing reduces alleviates responses promoting

Language: Английский

Citations

4