Biochemical and Biophysical Research Communications, Journal Year: 2024, Volume and Issue: 741, P. 151023 - 151023
Published: Nov. 19, 2024
Language: Английский
Biochemical and Biophysical Research Communications, Journal Year: 2024, Volume and Issue: 741, P. 151023 - 151023
Published: Nov. 19, 2024
Language: Английский
Journal of Neuroinflammation, Journal Year: 2025, Volume and Issue: 22(1)
Published: Jan. 21, 2025
Abstract Central nervous system (CNS) injuries, such as ischemic stroke (IS), intracerebral hemorrhage (ICH) and traumatic brain injury (TBI), are a significant global burden. The complex pathophysiology of CNS is comprised primary secondary injury. Inflammatory incited by damage-associated molecular patterns (DAMPs) which signal variety resident cells infiltrating immune cells. Extracellular cold-inducible RNA-binding protein (eCIRP) DAMP acts through multiple non-immune to promote inflammation. Despite the well-established role eCIRP in systemic sterile inflammation, its less elucidated. Recent literature suggests that pleiotropic inflammatory mediator also being evaluated clinical biomarker indicate prognosis injuries. This review provides broad overview injury, with focus on immune-mediated neuroinflammation. We then what known about mechanisms both non-CNS cells, identifying opportunities for further study. explore eCIRP’s potential prognostic marker severity outcome. Next, we provide an eCIRP-targeting therapeutics suggest strategies develop these agents ameliorate Finally, emphasize exploring novel mechanisms, aside from neuroinflammation, critical therapeutic target
Language: Английский
Citations
2International Journal of Molecular Medicine, Journal Year: 2025, Volume and Issue: 55(3)
Published: Jan. 21, 2025
Ischemic stroke, a leading cause of disability and mortality worldwide, is characterized by the sudden loss blood flow in specific area brain. Intravenous thrombolysis with recombinant tissue plasminogen activator only approved pharmacological treatment for acute ischemic stroke; however, aforementioned has significant clinical limitations, thus there an urgent need development novel mechanisms therapeutic strategies stroke. Astrocytes, abundant versatile cells central nervous system, offer crucial support to neurons nutritionally, structurally physically. They also contribute blood‑brain barrier formation regulate neuronal extracellular ion concentrations. Accumulated evidence revealed involvement astrocytes regulation host neurotransmitter metabolism, immune response repair, different metabolic characteristics can process suggesting that targeted astrocyte reprogramming may prognosis In present review, current understanding multifaceted along its regulatory factors pathways, as well promote polarization balance, which hold promise immunometabolism‑targeted therapies were summarized.
Language: Английский
Citations
1Molecular Neurobiology, Journal Year: 2024, Volume and Issue: unknown
Published: Aug. 6, 2024
Language: Английский
Citations
6Molecular Biology Reports, Journal Year: 2025, Volume and Issue: 52(1)
Published: April 1, 2025
Language: Английский
Citations
0ACS Chemical Neuroscience, Journal Year: 2025, Volume and Issue: unknown
Published: April 28, 2025
Excessive activation of microglia contributes to neuronal damage and astrocytic during cerebral ischemia hypoxia. Poliumoside (Pol) is a caffeoylated phenylpropanoid glycoside with significant anti-inflammatory antioxidant functions. However, whether Pol can mediate microglia-mediated neurotoxicity in the ischemic brain remains nebulous. Here, ischemia-reperfusion injury (CI/RI) mouse model was conducted investigate Pol's role microglial neurotoxicity. We found that significantly reduced neurological deficits, infarction volume, CI/RI model. inhibited proinflammatory cytokines activation, while enhancing cytokines. Mechanistically, markedly suppressed Fstl1, NF-κB phosphorylation, Nlrp3-Asc-Caspase1 inflammasome. In oxygen-glucose-deprivation (OGD)-mediated BV2 microglia, Fstl1 overexpression enhanced activation. The conditioned medium Fstl1-overexpressed promoted injuries. treatment or pathway inhibition reversed Fstl1-mediated effects. conclusion, restrained microglia-modulated neuroinflammation hypoxic-ischemic by restraining Fstl1-NF-κB pathway.
Language: Английский
Citations
0IBRO Neuroscience Reports, Journal Year: 2025, Volume and Issue: unknown
Published: April 1, 2025
Language: Английский
Citations
0Biochemical and Biophysical Research Communications, Journal Year: 2024, Volume and Issue: 741, P. 151023 - 151023
Published: Nov. 19, 2024
Language: Английский
Citations
1