Crosstalk Between the Oxidative Stress and Glia Cells After Stroke: From Mechanism to Therapies DOI Creative Commons

Ganggui Zhu,

Xiaoyu Wang, Luxi Chen

et al.

Frontiers in Immunology, Journal Year: 2022, Volume and Issue: 13

Published: Feb. 25, 2022

Stroke is the second leading cause of global death and characterized by high rates mortality disability. Oxidative stress accompanied other pathological processes that together lead to secondary brain damage in stroke. As major component brain, glial cells play an important role normal development injury processes. Multiple connections exist pathophysiological changes reactive oxygen species (ROS) metabolism glia cell activation. Astrocytes microglia are rapidly activated after stroke, generating large amounts ROS via mitochondrial NADPH oxidase pathways, causing oxidative themselves neurons. Meanwhile, alterations morphology function, mediate their processes, such as neuroinflammation, excitotoxicity, blood-brain barrier damage. In contrast, protect Central Nervous System (CNS) from synthesizing antioxidants regulating Nuclear factor E2-related 2 (Nrf2) pathway, among others. Although numerous previous studies have focused on immune function cells, little attention has been paid stress. this paper, we discuss adverse consequences production oxidative-antioxidant imbalance addition, further describe biological potential therapeutic tools based cells.

Language: Английский

Role of neuroinflammation in neurodegeneration development DOI Creative Commons
Weifeng Zhang, Dan Xiao, Qinwen Mao

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2023, Volume and Issue: 8(1)

Published: July 12, 2023

Abstract Studies in neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease and Amyotrophic lateral sclerosis, Huntington’s so on, have suggested that inflammation is not only a result of neurodegeneration but also crucial player this process. Protein aggregates which are very common pathological phenomenon can induce neuroinflammation further aggravates protein aggregation neurodegeneration. Actually, even happens earlier than aggregation. Neuroinflammation induced by genetic variations CNS cells or peripheral immune may deposition some susceptible population. Numerous signaling pathways range been to be involved the pathogenesis neurodegeneration, although they still far from being completely understood. Due limited success traditional treatment methods, blocking enhancing inflammatory considered promising strategies for therapy many them got exciting results animal models clinical trials. Some them, few, approved FDA usage. Here we comprehensively review factors affecting major pathogenicity sclerosis. We summarize current strategies, both clinic, diseases.

Language: Английский

Citations

545
NF-κB in biology and targeted therapy: new insights and translational implications DOI Creative Commons
Qing Guo, Yizi Jin, Xinyu Chen

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2024, Volume and Issue: 9(1)

Published: March 4, 2024

Abstract NF-κB signaling has been discovered for nearly 40 years. Initially, was identified as a pivotal pathway in mediating inflammatory responses. However, with extensive and in-depth investigations, researchers have that its role can be expanded to variety of mechanisms, biological processes, human diseases, treatment options. In this review, we first scrutinize the research process signaling, summarize composition, activation, regulatory mechanism signaling. We investigate interaction other important pathways, including PI3K/AKT, MAPK, JAK-STAT, TGF-β, Wnt, Notch, Hedgehog, TLR The physiological pathological states well intricate involvement inflammation, immune regulation, tumor microenvironment, are also explicated. Additionally, illustrate how is involved cancers, autoimmune cardiovascular metabolic neurological COVID-19. Further, discuss therapeutic approaches targeting IKK inhibitors, monoclonal antibodies, proteasome nuclear translocation DNA binding TKIs, non-coding RNAs, immunotherapy, CAR-T. Finally, provide an outlook field hope present stereoscopic, comprehensive will inform future clinical practice.

Language: Английский

Citations

423
Function and therapeutic value of astrocytes in neurological diseases DOI
Hong‐Gyun Lee, Michael A. Wheeler, Francisco J. Quintana

et al.

Nature Reviews Drug Discovery, Journal Year: 2022, Volume and Issue: 21(5), P. 339 - 358

Published: Feb. 16, 2022

Language: Английский

Citations

364
Microglia and Central Nervous System–Associated Macrophages—From Origin to Disease Modulation DOI
Marco Prinz, Takahiro Masuda, Michael A. Wheeler

et al.

Annual Review of Immunology, Journal Year: 2021, Volume and Issue: 39(1), P. 251 - 277

Published: Feb. 9, 2021

The immune system of the central nervous (CNS) consists primarily innate cells. These are highly specialized macrophages found either in parenchyma, called microglia, or at CNS interfaces, such as leptomeningeal, perivascular, and choroid plexus macrophages. While they were thought phagocytes, their function extends well beyond simple removal cell debris during development diseases. Brain-resident cells to be plastic, long-lived, host an outstanding number risk genes for multiple pathologies. As a result, now considered most suitable targets modulating Additionally, recent single-cell technologies enhanced our molecular understanding origins, fates, interactomes, functional statesduring health perturbation. Here, we review current state challenges myeloid biology treatment options related

Language: Английский

Citations

353
Gut-licensed IFNγ+ NK cells drive LAMP1+TRAIL+ anti-inflammatory astrocytes DOI
Liliana M. Sanmarco, Michael A. Wheeler, Cristina Gutiérrez‐Vázquez

et al.

Nature, Journal Year: 2021, Volume and Issue: 590(7846), P. 473 - 479

Published: Jan. 6, 2021

Language: Английский

Citations

240
Functional roles of reactive astrocytes in neuroinflammation and neurodegeneration DOI
Rickie Patani, Giles E. Hardingham, Shane A. Liddelow

et al.

Nature Reviews Neurology, Journal Year: 2023, Volume and Issue: 19(7), P. 395 - 409

Published: June 12, 2023

Language: Английский

Citations

235
Astrocytic interleukin-3 programs microglia and limits Alzheimer’s disease DOI
Cameron S. McAlpine, Joseph Park,

Ana Griciuc

et al.

Nature, Journal Year: 2021, Volume and Issue: 595(7869), P. 701 - 706

Published: July 14, 2021

Language: Английский

Citations

233
The Immune Response in Multiple Sclerosis DOI

Sofía Rodríguez Murúa,

Mauricio Farez, Francisco J. Quintana

et al.

Annual Review of Pathology Mechanisms of Disease, Journal Year: 2021, Volume and Issue: 17(1), P. 121 - 139

Published: Oct. 4, 2021

Multiple sclerosis (MS) is a chronic autoimmune, inflammatory, and neurodegenerative disease that affects the central nervous system (CNS). MS characterized by immune dysregulation, which results in infiltration of CNS cells, triggering demyelination, axonal damage, neurodegeneration. Although exact causes are not fully understood, genetic environmental factors thought to control onset progression. In this article, we review main immunological mechanisms involved pathogenesis.

Language: Английский

Citations

218
Barcoded viral tracing of single-cell interactions in central nervous system inflammation DOI
Iain C. Clark, Cristina Gutiérrez‐Vázquez, Michael A. Wheeler

et al.

Science, Journal Year: 2021, Volume and Issue: 372(6540)

Published: April 22, 2021

Single-cell analysis of CNS interactions Despite their importance in the physiology and pathology central nervous system (CNS), few methods are available for unbiased, systematic investigation cell-to-cell at single-cell resolution. Clark et al. developed RABID-seq, a method that combines barcoded viral tracing with RNA sequencing (see Perspective by Silvin Ginhoux). RABID-seq identified axon guidance molecules Sema4D-PlexinB2 EphrinB3-EphB3 as mediators microglia-astrocyte promote experimental autoimmune encephalomyelitis and, potentially, multiple sclerosis. These studies also candidate therapeutic modulation Science , this issue p. eabf1230 ; see 342

Language: Английский

Citations

205
Neuroinflammation in Alzheimer’s Disease DOI Creative Commons
Isaac G. Onyango, Gretsen Velezmoro Jáuregui, Mária Čarná

et al.

Biomedicines, Journal Year: 2021, Volume and Issue: 9(5), P. 524 - 524

Published: May 7, 2021

Alzheimer's disease (AD) is a neurodegenerative associated with human aging. Ten percent of individuals over 65 years have AD and its prevalence continues to rise increasing age. There are currently no effective modifying treatments for AD, resulting in increasingly large socioeconomic personal costs. Increasing age an increase low-grade chronic inflammation (inflammaging) that may contribute the process AD. Although exact mechanisms remain unclear, aberrant elevation reactive oxygen nitrogen species (RONS) levels from several endogenous exogenous processes brain not only affect cell signaling, but also trigger cellular senescence, inflammation, pyroptosis. Moreover, compromised immune privilege allows infiltration peripheral cells infectious agents play role. Additionally, meta-inflammation as well gut microbiota dysbiosis drive neuroinflammatory process. Considering inflammatory/immune pathways dysregulated parallel cognitive dysfunction elucidating relationship between central nervous system facilitate development safe therapy We discuss some current ideas on inflammaging appear summarize details few immunomodulatory strategies being developed selectively target detrimental aspects neuroinflammation without affecting defense against pathogens tissue damage.

Language: Английский

Citations

204