Immunomodulation: The next target of mesenchymal stem cell-derived exosomes in the context of ischemic stroke DOI Creative Commons
Xiaoqian Shan, Yongyin Luo, Jun Chang

et al.

World Journal of Stem Cells, Journal Year: 2023, Volume and Issue: 15(3), P. 52 - 70

Published: March 22, 2023

Ischemic stroke (IS) is the most prevalent form of brain disease, characterized by high morbidity, disability, and mortality. However, there still a lack ideal prevention treatment measures in clinical practice. Notably, transplantation therapy mesenchymal stem cells (MSCs) has been hot research topic stroke. Nevertheless, are risks associated with this cell therapy, including tumor formation, coagulation dysfunction, vascular occlusion. Also, growing number studies suggest that therapeutic effect after MSCs mainly attributed to MSC-derived exosomes (MSC-Exos). And cell-free mediated appears circumvent many difficulties when compared it may be promising new strategy for treating as replacement therapy. Studies suppressing inflammation via modulation immune response an additional option IS. Intriguingly, MSC-Exos mediates inflammatory following IS modulating central nervous system, peripheral immunomodulatory molecules, thereby promoting neurofunctional recovery Thus, paper reviews role, potential mechanisms, post-IS order identify targets.

Language: Английский

Inflammation and the Link to Vascular Brain Health: Timing Is Brain DOI Open Access

Katherine T Mun,

Jason D. Hinman

Stroke, Journal Year: 2022, Volume and Issue: 53(2), P. 427 - 436

Published: Jan. 10, 2022

Inflammation and its myriad pathways are now recognized to play both causal consequential roles in vascular brain health. From acting as a trigger for injury, evidenced by the COVID-19 pandemic, steadily increasing risk chronic cerebrovascular disease, distinct inflammatory cascades differential varying states of injury. New evidence is regularly emerging that characterizes role specific these including those at stroke injury well during acute, subacute, repair phases stroke. Here, we aim highlight recent basic science clinical many active The infections, spotlighted severe acute respiratory syndrome coronavirus 2 association with increased also reviewed. Rather than converging on shared mechanism, studies implicate varied processes repair. Recognition phasic nature disease likely essential development implementation an anti-inflammatory strategy prevention, treatment, Although advances revascularization have taught us time brain, targeting inflammation treatment will undoubtedly show timing brain.

Language: Английский

Citations

33

Signaling pathways in brain ischemia: Mechanisms and therapeutic implications DOI

Wen Lin,

Xiaosu Zhao, Jiawen Cheng

et al.

Pharmacology & Therapeutics, Journal Year: 2023, Volume and Issue: 251, P. 108541 - 108541

Published: Oct. 1, 2023

Language: Английский

Citations

21

The interaction between intestinal microenvironment and stroke DOI Creative Commons
Linna Zhao, Jie Xiao, Song‐Lin Li

et al.

CNS Neuroscience & Therapeutics, Journal Year: 2023, Volume and Issue: 29(S1), P. 185 - 199

Published: June 1, 2023

Background Stroke is not only a major cause of disability but also the third leading death, following heart disease and cancer. It has been established that stroke causes permanent in 80% survivors. However, current treatment options for this patient population are limited. Inflammation immune response features well‐recognized to occur after stroke. The gastrointestinal tract hosts complex microbial communities, largest pool cells, forms bidirectional regulation brain‐gut axis with brain. Recent experimental clinical studies have highlighted importance relationship between intestinal microenvironment Over years, influence intestine on emerged as an important dynamic research direction biology medicine. Aims In review, we describe structure function highlight its cross‐talk addition, discuss potential strategies aiming target during treatment. Conclusion environment can neurological cerebral ischemic outcome. Improving by targeting gut microbiota may be new treating

Language: Английский

Citations

19

Mechanism of PGC-1α-mediated mitochondrial biogenesis in cerebral ischemia–reperfusion injury DOI Creative Commons
Ying Yuan, Yuan Tian, Hui Jiang

et al.

Frontiers in Molecular Neuroscience, Journal Year: 2023, Volume and Issue: 16

Published: July 10, 2023

Cerebral ischemia–reperfusion injury (CIRI) is a series of cascade reactions that occur after blood flow recanalization in the ischemic zone patients with cerebral infarction, causing an imbalance intracellular homeostasis through multiple pathologies such as increased oxygen free radicals, inflammatory response, calcium overload, and impaired energy metabolism, leading to mitochondrial dysfunction ultimately apoptosis. Rescue reversibly damaged neurons hemispheric key saving brain infarction reducing neurological deficits. Complex active functions are highly dependent on adequate supply from mitochondria. Mitochondrial biogenesis (MB), process generates new functional mitochondria restores normal function by replacing mitochondria, major mechanism for maintaining intra-mitochondrial involved quality control ameliorate thus protects against CIRI. The main regulator MB peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α), which improves protect CIRI activating its downstream nuclear respiratory factor 1 (NRF1) transcription A (TFAM) promote genome replication transcription. This paper provides theoretical reference treatment impairment caused discussing mechanisms during injury.

Language: Английский

Citations

18

The interplay between ferroptosis and inflammation: therapeutic implications for cerebral ischemia-reperfusion DOI Creative Commons
Yuxuan He, Jingyi Wang,

Chun-Miao Ying

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Nov. 8, 2024

Stroke ranks as the second most significant contributor to mortality worldwide and is a major factor in disability. Ischemic strokes account for 71% of all stroke incidences globally. The foremost approach treating ischemic prioritizes quick reperfusion, involving methods such intravenous thrombolysis endovascular thrombectomy. These techniques can reduce disability but necessitate immediate intervention. After cerebral ischemia, inflammation rapidly arises vascular system, producing pro-inflammatory signals that activate immune cells, which turn worsen neuronal injury. Following an overload intracellular iron triggers Fenton reaction, resulting excess free radicals cause lipid peroxidation damage cellular membranes, ultimately leading ferroptosis. relationship between ferroptosis increasingly recognized vital process ischemia-reperfusion (I/R). Inflammatory processes disturb balance encourage (LPO) through neuroglial while also reducing activity antioxidant systems, contributing Furthermore, products generated during ferroptosis, along with damage-associated molecular patterns (DAMPs) released from ruptured cell incite inflammation. Given complex inflammation, investigating their interaction brain I/R crucial understanding disease development creating innovative therapeutic options. Consequently, this article will provide comprehensive introduction mechanisms linking neuroinflammation, well evaluate potential treatment modalities, goal presenting various insights alleviating injury exploring new avenues.

Language: Английский

Citations

7

Ischemic Stroke, Glucocorticoids, and Remote Hippocampal Damage: A Translational Outlook and Implications for Modeling DOI Creative Commons
N. V. Gulyaeva, М. В. Онуфриев,

Yulia V. Moiseeva

et al.

Frontiers in Neuroscience, Journal Year: 2021, Volume and Issue: 15

Published: Dec. 9, 2021

Progress in treating ischemic stroke (IS) and its delayed consequences has been frustratingly slow due to the insufficient knowledge on mechanism. One important factor, hypothalamic-pituitary-adrenocortical (HPA) axis is mostly neglected despite fact that both clinical data results from rodent models of IS show glucocorticoids, hormones this stress axis, are involved IS-induced brain dysfunction. Though increased cortisol regarded as a biomarker higher mortality worse recovery prognosis, detailed mechanisms HPA dysfunction involvement post-stroke cognitive emotional disorders remain obscure. In review, we analyze alterations supposed association corticoid-dependent distant hippocampal damage disorders. A translationally growing point bridging gap between pathogenesis clinic investigate disturbances related at different stages SI. Valid reproduce state cases needed, should be considered when planning pre-clinical research. studies IS, it useful reinforce diagnostic prognostic potential other hormones. Finally, reveal patients with permanently disturbed axis. Patients-at-risk high prone remote monitored since may basis for development disturbances, well epilepsy.

Language: Английский

Citations

34

Research progress on pyroptosis-mediated immune-inflammatory response in ischemic stroke and the role of natural plant components as regulator of pyroptosis: A review DOI Creative Commons
Kailin Yang, Tingting Bao, Jinsong Zeng

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2022, Volume and Issue: 157, P. 113999 - 113999

Published: Nov. 28, 2022

Ischemic stroke (IS) is one of the leading causes death and disability. Its pathogenesis not completely clear, inflammatory cascade its main pathological processes. The current clinical practice IS to restore blood supply ischemic area after as soon possible through thrombolytic therapy protect vitality function neurons. However, reperfusion further accelerates damage cause ischemia-reperfusion injury. process cerebral injury involves multiple mechanisms, exact mechanism has been fully elucidated. Pyroptosis, a newly discovered form programmed cell death, plays an important role in initiation progression inflammation. It pro-inflammatory mediated by caspase Caspase-1/4/5/11, which can lead swelling rupture, release factors IL-1β IL-18, induce cascade. Recent studies have shown that pyroptosis response are aggravating brain injury, inhibition may alleviate Furthermore, found natural plant components regulatory effect on pyroptosis. Therefore, this review only summarizes molecular stroke, but also regulator pyroptosis, order provide reference information for treatment future.

Language: Английский

Citations

23

Inhibition of mitochondrial VDAC1 oligomerization alleviates apoptosis and necroptosis of retinal neurons following OGD/R injury DOI
Hao Wan,

Yan-di Yan,

Xi‐min Hu

et al.

Annals of Anatomy - Anatomischer Anzeiger, Journal Year: 2023, Volume and Issue: 247, P. 152049 - 152049

Published: Jan. 20, 2023

Language: Английский

Citations

16

TRIM67 alleviates cerebral ischemia‒reperfusion injury by protecting neurons and inhibiting neuroinflammation via targeting IκBα for K63-linked polyubiquitination DOI Creative Commons
Yongbo Yu, Qian Xia,

Gaofeng Zhan

et al.

Cell & Bioscience, Journal Year: 2023, Volume and Issue: 13(1)

Published: May 29, 2023

Abstract Background Excessive and unresolved neuroinflammation plays an important role in the pathophysiology of many neurological disorders, such as ischemic stroke, yet there are no effective treatments. Tripartite motif-containing 67 (TRIM67) a crucial control inflammatory disease pathogen infection-induced inflammation; however, TRIM67 cerebral ischemia‒reperfusion injury remains poorly understood. Results In present study, we demonstrated that expression level was significantly reduced middle artery occlusion reperfusion (MCAO/R) mice primary cultured microglia subjected to oxygen–glucose deprivation reperfusion. Furthermore, significant reduction infarct size deficits observed after upregulation. Interestingly, upregulation alleviated cell death MCAO/R mice. A mechanistic study showed bound IκBα, K48-linked ubiquitination increased K63-linked ubiquitination, thereby inhibiting its degradation promoting stability ultimately NF-κB activity ischemia. Conclusion Taken together, this previously unidentified mechanism whereby regulates neuronal apoptosis strongly indicates may provide therapeutic benefits for stroke. Graphical

Language: Английский

Citations

14

Association of multiple sclerosis with stroke: A comprehensive review DOI Creative Commons
Mohammed Dheyaa Marsool Marsool, Priyadarshi Prajjwal, Jobby John

et al.

Health Science Reports, Journal Year: 2024, Volume and Issue: 7(1)

Published: Jan. 1, 2024

Abstract Background Multiple sclerosis (MS) is a chronic immune‐mediated disorder characterized by the degradation of myelin sheath in central nervous system. Research indicates that individuals with MS exhibit higher susceptibility to stroke compared general population. This association rooted shared underlying mechanisms, specifically involving neuroinflammatory processes. Methodology We performed an extensive search on PubMed, MEDLINE, Embase, Scopus, and Google Scholar using specific terms. The terms included variations “multiple sclerosis,” “stroke,” “cerebrovascular disease,” “vascular risk factors,” “disease‐modifying therapies,” “neuroinflammation.” was limited articles published from January 1, 2000, up 31 May, 2023. Results Discussion Stroke, global health burden significant mortality adult disability, underscores critical importance understanding link between stroke. Despite growing body research establishing elevated patients, notable information gaps persist. Limited prospective multicenter studies incidence patients contribute incomplete precise relationship these two conditions. Conclusion In conclusion, this review need for thorough complex identified factors influence DMTs necessitate further investigation inform evidence‐based preventive therapeutic strategies. Bridging existing through imperative comprehensive association. development targeted diagnostic approaches acute paramount mitigate impact debilitating Ultimately, serves as foundation future efforts enhance preventative measures interventions, thereby improving overall quality life susceptible strokes.

Language: Английский

Citations

6