Interplay of cell death pathways and immune responses in ischemic stroke: insights into novel biomarkers DOI
Arian Daneshpour, Zoha Shaka, Nima Rezaei

et al.

Reviews in the Neurosciences, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 16, 2024

Abstract Stroke is a severe neurological disease and major worldwide issue, mostly manifesting as ischemic stroke (IS). In order to create effective treatments for IS, it imperative fully understand the underlying pathologies, existing therapeutic choices are inadequate. Recent investigations have shown complex relationships between several programmed cell death (PCD) pathways, including necroptosis, ferroptosis, pyroptosis, their correlation with immune responses during IS. However, this relationship still unclear. To address gap, review study explored cellular interactions in microenvironment of Then, validate prior findings uncover biomarkers, investigated bioinformatics studies. Several nuclear factor kappa-light-chain-enhancer activated B cells (NF-κB), Toll-like receptor 4 (TLR4), receptor-interacting protein kinase (RIPK), were involved PCD-immune interactions. The studies reported key biomarkers such glutathione peroxidase (GPX4), NOD-like family pyrin domain containing 3 (NLRP3), gasdermin D (GSDMD), TLR4, which important implications cuproptosis, necroptosis respectively. These associated PCD mechanisms oxidative stress inflammatory reactions. infiltration analysis consistently revealed significant pathways detrimental cells, neutrophils γδ T cells. Conversely, M2 macrophages helper showed protective effects. conclusion, considering intricate network emphasized necessity paradigm shift approaches injuries that related network.

Language: Английский

Lymphocyte Subset Imbalance in Cardiometabolic Diseases: Are T Cells the Missing Link? DOI Open Access

Francesca Picone,

Valentina Giudice, Concetta Iside

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(3), P. 868 - 868

Published: Jan. 21, 2025

Cardiometabolic and cardiovascular diseases (CVDs) remain the leading cause of death worldwide, with well-established risk factors such as smoking, obesity, diabetes contributing to plaque formation chronic inflammation. However, emerging evidence suggests that immune system plays a more significant role in development progression CVD than previously thought. Specifically, finely tuned regulation lymphocyte subsets governs post-injury inflammation tissue damage resolution orchestrates functions activation endothelial cells, cardiomyocytes, fibroblasts CVD-associated lesions (e.g., atherosclerotic plaques). A deeper understanding system’s involvement will provide new insights into disease biology uncover novel therapeutic targets aimed at re-establishing homeostasis. In this review, we summarize current state knowledge on distribution CVD, including atherosclerosis, diabetes, hypertension, myocardial infarction, stroke.

Language: Английский

Citations

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Long Noncoding RNA ISA1 Protects Against Ischemic Brain Damage by Promoting the Transformation of Microglia Toward Anti-inflammatory Phenotype via the SOCS3/JAK2/STAT3 Pathway DOI

Ermei Lu,

Peng Zhou, Yuanyuan Li

et al.

Neurochemical Research, Journal Year: 2025, Volume and Issue: 50(2)

Published: Feb. 1, 2025

Language: Английский

Citations

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Blocking S1P4 signaling attenuates brain injury in mice with ischemic stroke DOI Creative Commons
Nikita Basnet, Hyun-kyung Cho,

Arjun Sapkota

et al.

Journal of Advanced Research, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 1, 2025

Language: Английский

Citations

0
Therapeutic Potential of TPT-260 in Ischemic Stroke: An Investigation Into Its Anti-Inflammatory Effects and Impact on Microglial Activation DOI Creative Commons

Jun Qian,

Xiaoming Guo, Xu Qian

et al.

Journal of Inflammation Research, Journal Year: 2025, Volume and Issue: Volume 18, P. 3055 - 3066

Published: March 1, 2025

Ischemic stroke is characterized by a high incidence and elevated mortality. events trigger neuroinflammation, leading to severe brain edema neuronal necrosis. Microglia are the primary mediators of neuroinflammation. Inhibition M1 microglia effectively alleviate damage in mild stroke. TPT-260 minimally cytotoxic, small molecule chaperone retromer complex, which mediates recycling trafficking membrane protein receptors. This study explores therapeutic effects related mechanisms model mice from an anti-inflammatory perspective, aiming evaluate efficacy mechanism treating In this study, middle cerebral artery occlusion (MCAO) animal was established simulate ischemic Primary were cultured for lipopolysaccharides treatment construct microglia. Both animals cells treated with TPT-260. Nuclear factor-κB (NF-κB) nuclear translocation expression downstream pro-inflammatory factors Interleukin 1β (IL-1β) Tumor necrosis factor-α (TNF-α) determined. vivo results revealed that significantly reduced infarct area inflammation as well improved neurological function mice. The potential involved marked inhibition lipopolysaccharides-induced suppressing NF-κB attenuating IL-1β TNF-α. Moreover, inhibited NOD-like receptor 3 inflammasome formation, thereby decreasing release mature alleviating attenuated via repression signaling, thus preventing neuroinflammation injuries

Language: Английский

Citations

0
Procyanidins for the treatment of Parkinson's disease and ischemic stroke DOI
Weiran Li, Xinying Li, Pingping Wang

et al.

Journal of Functional Foods, Journal Year: 2025, Volume and Issue: 127, P. 106717 - 106717

Published: March 12, 2025

Language: Английский

Citations

0
Targeting to miR-130b-5p/TLR4: How sodium danshensu suppresses inflammatory response of microglia in cerebral ischemia-reperfusion injury DOI
Lin Guo, Miao Zeng, Guangming Zhang

et al.

International Immunopharmacology, Journal Year: 2025, Volume and Issue: 153, P. 114497 - 114497

Published: March 22, 2025

Language: Английский

Citations

0
Neuroprotective mechanisms of microglia in ischemic stroke: a review focused on mitochondria DOI
Jianhua Gan, Xinyi Yang, Jianan Wu

et al.

Molecular Biology Reports, Journal Year: 2025, Volume and Issue: 52(1)

Published: April 1, 2025

Language: Английский

Citations

0
Aerobic exercise, an effective intervention for cognitive impairment after ischemic stroke DOI Creative Commons
Mingjin Zhu, Wenjun Chen, Jie Zhang

et al.

Frontiers in Aging Neuroscience, Journal Year: 2025, Volume and Issue: 17

Published: April 4, 2025

Cognitive dysfunction is a common and debilitating complication following ischemic stroke, significantly impairing the quality of life patients. In recent years, aerobic exercise has emerged as promising non-pharmacological intervention to mitigate post-stroke cognitive impairment (PSCI). This review synthesizes current evidence on efficacy mechanisms in enhancing recovery after stroke. Key include improved cerebral hemodynamics through enhanced blood flow (CBF), promotion neuroplasticity via brain-derived neurotrophic factor (BDNF)-mediated pathways, suppression neuroinflammation (e.g., NLRP3 inflammasome inhibition), attenuation oxidative stress. Preclinical clinical studies demonstrate that modalities such gait training, cycling, aquatic therapy enhance domains including memory, executive function, attention, with optimal benefits observed at moderate-to-high intensity frequency ≥3 sessions per week. Despite robust evidence, challenges remain standardizing protocols addressing individual variability treatment response. Future research should prioritize large-scale randomized controlled trials validate long-term identify biomarkers for personalized rehabilitation strategies. underscores imperative integrate into paradigms, offering dual therapeutic approach improve both physical outcomes.

Language: Английский

Citations

0
FCGR1A Alleviates Ischemic Stroke-induced Injury by Promoting Anti-Inflammatory Microglial Polarization via the AMPK–mTOR Signaling Pathway DOI Creative Commons
Meng Liu,

Xiang‐Bing Fan,

D Chen

et al.

Frontiers in Bioscience-Landmark, Journal Year: 2025, Volume and Issue: 30(5)

Published: April 29, 2025

Ischemic stroke triggers inflammatory responses that lead to neuronal damage, with microglial polarization significantly influencing post-stroke inflammation. This study explores the role of Fc gamma receptor Ia (FCGR1A) in and its regulatory mechanisms ischemic stroke. Differentially expressed genes (DEGs) associated were identified using GSE58294 dataset. Hub found by analyzing protein-protein interaction (PPI) networks. BV2 microglia subjected oxygen-glucose deprivation/reoxygenation (OGD/R) mimic conditions vitro, FCGR1A marker levels assessed. Besides, cells stimulated lipopolysaccharide (LPS) interferon-gamma (IFN-γ) induce M1 polarization, effects overexpression knockdown on cytokine production evaluated. The function AMP-activated protein kinase (AMPK)-mTOR pathway regulating was further investigated mTOR inhibitor rapamycin (RAP). From 327 DEGs identified, chosen as a hub gene. OGD/R treatment produced time-dependent rise FCGR1A, induction brown adipocytes 1 (Iba1), interleukin 6 (IL-6) expression, indicating enhanced induced proinflammatory response promoted whereas reduced inflammation shifted toward an anti-inflammatory M2 phenotype. Inhibition RAP, combined knockdown, AMPK activation shift modulates affecting AMPK-mTOR signaling conditions. Targeting related pathways could offer new therapeutic strategies lessen facilitate healing process after

Language: Английский

Citations

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Targeting CD74 in microglia to modulate experimental cerebral ischemia and reperfusion injury: insights from Single-Cell and bulk transcriptomics DOI Creative Commons
Chang Cao, Tengteng Liu, Peng Lü

et al.

Molecular Brain, Journal Year: 2025, Volume and Issue: 18(1)

Published: May 21, 2025

Language: Английский

Citations

0