FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4387060894> ?p ?o ?g. }

• W4387060894 abstract "Multiple sclerosis (MS) is the most common inflammatory neurodegenerative disease in young adults, resulting in neurological defects and disability. The endogenous mechanisms to resolve inflammation are intact but become defective in patients, resulting in lack of resolution mediators and unresolved chronic inflammation. Docosahexaenoic acid (DHA) metabolism being impaired in MS, we hypothesize that supplementing its downstream metabolite maresin 1 (MaR1) will alleviate inflammation and demyelination in preclinical mouse model of MS; experimental allergic encephalomyelitis (EAE). Restoration of MaR1 by its exogenous administration in EAE mice propagated inflammatory resolution and had a protective effect on neurological deficits, prevented disease progression, and reduced disease severity by reducing immune cell infiltration (CD4+IL17+ and CD4+IFN-γ+) into the CNS. It significantly reduced the proinflammatory cytokine IL17 and promoted an anti-inflammatory response via IL10 and IL4. Neutralization of IL10 abolished the protective effect of MaR1 in EAE confirming IL10 is mediating MaR1 effect in EAE. Furthermore, it improved the pathophysiology and exerted neuroprotective effects by mitigating disease signs in EAE as evidenced by lower levels of NFL in the plasma of treated group compared to control and higher MBP expression in the brain from the MaR1 treated mice, decreased inflammatory infiltrates, and less demyelination and vacuolization in the spinal cord tissue sections of treated mice. SCENITH data confirmed that MaR1 maintains myelin by regulating oligodendrocyte metabolism. Also, it induces metabolic reprogramming in infiltrating CD4 cells and macrophages, which modulate their phenotype. Metabolic changes induced macrophages by MaR1 restores the impaired efferocytosis in EAE, promoting clearance of damaged myelin and dead cells; thereby lowering the disability with disease course. Overall, MaR1 supplementation has anti-inflammatory and neuroprotective effects in preclinical animal models and induces metabolic reprogramming in disease associated cell-types, promotes efferocytosis, implying that it could be a new therapeutic molecule in MS and other autoimmune diseases.Inflammation is dysregulated in EAE due to impaired synthesis of DHA derived proresolving lipid mediator MaR1.Administration of the resolution agonist MaR1 propagates resolution processes and improves neurological outcome in RR model of EAE.MaR1 ameliorates clinical signs of EAE by attenuating pro-inflammatory cytokine IL17 mediated response and promoting anti-inflammatory response through IL10.MaR1 supplementation improves the pathophysiology in EAE and shows neuroprotection as indicated by the lower levels of NFL in the plasma and higher expression of MBP in the brain of treated mice.MaR1 induces metabolic reprogramming in disease-associated cell types.MaR1 promotes efferocytosis in EAE through metabolic reprogramming of macrophages.Inflammatory process is a protective response to several challenges like injury or infection. However, it must resolve over time to maintain tissue homeostasis. Impaired or delayed resolution leads to damaging effects, including chronic inflammation, tissue damage, and disease progression as occurs in multiple sclerosis (MS). We report that inflammation is dysregulated in preclinical animal model of MS, experimental autoimmune encephalomyelitis (EAE), partially due to impaired synthesis of proresolving lipid mediators. We show that the administration of the resolution agonist known as maresin 1 (MaR1) in EAE actively propagates resolution processes and improves neurological outcome. We conclude that MaR1 is a potential interventional candidate to attenuate dysregulated inflammation and to restore neurological deficits in EAE." @default.
• W4387060894 created "2023-09-27" @default.
• W4387060894 creator A5018695538 @default.
• W4387060894 creator A5030868660 @default.
• W4387060894 creator A5031007874 @default.
• W4387060894 creator A5032387130 @default.
• W4387060894 creator A5038457825 @default.
• W4387060894 creator A5051644112 @default.
• W4387060894 creator A5054743305 @default.
• W4387060894 creator A5074447378 @default.
• W4387060894 creator A5074885471 @default.
• W4387060894 creator A5086871265 @default.
• W4387060894 creator A5089281134 @default.
• W4387060894 date "2023-09-26" @default.
• W4387060894 modified "2023-10-14" @default.
• W4387060894 title "Pro-resolution lipid mediator maresin-1 ameliorates inflammation, promotes neuroprotection, and prevents disease progression in experimental models of multiple sclerosis" @default.
• W4387060894 cites W1739691545 @default.
• W4387060894 cites W1828576284 @default.
• W4387060894 cites W1964264880 @default.
• W4387060894 cites W1991273577 @default.
• W4387060894 cites W1992250154 @default.
• W4387060894 cites W1998496298 @default.
• W4387060894 cites W2000443242 @default.
• W4387060894 cites W2004536682 @default.
• W4387060894 cites W2008284866 @default.
• W4387060894 cites W2013234597 @default.
• W4387060894 cites W2017718617 @default.
• W4387060894 cites W2025714915 @default.
• W4387060894 cites W2030150321 @default.
• W4387060894 cites W2044359338 @default.
• W4387060894 cites W2048082433 @default.
• W4387060894 cites W2048167823 @default.
• W4387060894 cites W2082649626 @default.
• W4387060894 cites W2084476310 @default.
• W4387060894 cites W2090678790 @default.
• W4387060894 cites W2107277218 @default.
• W4387060894 cites W2118348421 @default.
• W4387060894 cites W2120699390 @default.
• W4387060894 cites W2130852003 @default.
• W4387060894 cites W2131726621 @default.
• W4387060894 cites W2146791037 @default.
• W4387060894 cites W2293276114 @default.
• W4387060894 cites W2467852101 @default.
• W4387060894 cites W2560140067 @default.
• W4387060894 cites W2585260788 @default.
• W4387060894 cites W2767429780 @default.
• W4387060894 cites W2772511794 @default.
• W4387060894 cites W2803312042 @default.
• W4387060894 cites W2806791998 @default.
• W4387060894 cites W2889599825 @default.
• W4387060894 cites W2901171936 @default.
• W4387060894 cites W2907223756 @default.
• W4387060894 cites W2911210789 @default.
• W4387060894 cites W2911658427 @default.
• W4387060894 cites W2985811865 @default.
• W4387060894 cites W2989664264 @default.
• W4387060894 cites W3029369961 @default.
• W4387060894 cites W3041707034 @default.
• W4387060894 cites W3108924494 @default.
• W4387060894 cites W3124687622 @default.
• W4387060894 cites W3173925204 @default.
• W4387060894 cites W3174064560 @default.
• W4387060894 cites W4205525405 @default.
• W4387060894 cites W4229016299 @default.
• W4387060894 cites W4237669910 @default.
• W4387060894 cites W4294316904 @default.
• W4387060894 cites W4321076018 @default.
• W4387060894 doi "https://doi.org/10.1101/2023.09.25.559216" @default.
• W4387060894 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37808700" @default.
• W4387060894 hasPublicationYear "2023" @default.
• W4387060894 type Work @default.
• W4387060894 citedByCount "0" @default.
• W4387060894 crossrefType "posted-content" @default.
• W4387060894 hasAuthorship W4387060894A5018695538 @default.
• W4387060894 hasAuthorship W4387060894A5030868660 @default.
• W4387060894 hasAuthorship W4387060894A5031007874 @default.
• W4387060894 hasAuthorship W4387060894A5032387130 @default.
• W4387060894 hasAuthorship W4387060894A5038457825 @default.
• W4387060894 hasAuthorship W4387060894A5051644112 @default.
• W4387060894 hasAuthorship W4387060894A5054743305 @default.
• W4387060894 hasAuthorship W4387060894A5074447378 @default.
• W4387060894 hasAuthorship W4387060894A5074885471 @default.
• W4387060894 hasAuthorship W4387060894A5086871265 @default.
• W4387060894 hasAuthorship W4387060894A5089281134 @default.
• W4387060894 hasBestOaLocation W43870608941 @default.
• W4387060894 hasConcept C134018914 @default.
• W4387060894 hasConcept C164027704 @default.
• W4387060894 hasConcept C203014093 @default.
• W4387060894 hasConcept C25498285 @default.
• W4387060894 hasConcept C2776914184 @default.
• W4387060894 hasConcept C2778486448 @default.
• W4387060894 hasConcept C2778609137 @default.
• W4387060894 hasConcept C2780640218 @default.
• W4387060894 hasConcept C529278444 @default.
• W4387060894 hasConcept C71924100 @default.
• W4387060894 hasConcept C98274493 @default.
• W4387060894 hasConceptScore W4387060894C134018914 @default.
• W4387060894 hasConceptScore W4387060894C164027704 @default.
• W4387060894 hasConceptScore W4387060894C203014093 @default.
• W4387060894 hasConceptScore W4387060894C25498285 @default.

• next