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GCH1 reduces LPS-induced alveolar macrophage polarization and inflammation by inhibition of ferroptosis
ConclusionsGCH1 inhibited ferroptosis in LPS-stimulated macrophages, reduced macrophage toward to M1 polarization and inflammatory response.
Source: Inflammation Research - September 21, 2023 Category: Research Source Type: research

USP10 regulates macrophage inflammation responses via stabilizing NEMO in LPS-induced sepsis
ConclusionsOverall, USP10 was shown to regulate inflammatory responses by stabilizing the NEMO protein, which may be a potential therapeutic target for sepsis-induced lung injury.
Source: Inflammation Research - July 12, 2023 Category: Research Source Type: research

Resveratrol-induced SIRT1 activation inhibits glycolysis-fueled angiogenesis under rheumatoid arthritis conditions independent of HIF-1 α
ConclusionGlycolysis provides additional energy to sustain Rho/ROCK activation in RA subjects, which promotes VEGF-driven angiogenesis and can be inhibited by SIRT1 activation.
Source: Inflammation Research - April 4, 2023 Category: Research Source Type: research

Inhibition of importin-7 attenuates ventilator-induced lung injury by targeting nuclear translocation of p38
ConclusionsOur findings uncover a key role for Imp7 in the process of p38 nuclear import after CS stimulation and highlight the potential of preventing p38 nuclear translocation in treatment of VILI.
Source: Inflammation Research - April 1, 2023 Category: Research Source Type: research

Annexin A1 (Ac2-26)-dependent Fpr2 receptor alleviates sepsis-induced acute kidney injury by inhibiting inflammation and apoptosis in vivo and in vitro
ConclusionsTaken together, this study provides evidence that the protective effect of ANXA1 (Ac2-26) on SI-AKI largely depends on the negative regulation of inflammation and apoptosis via the Fpr2 receptor.
Source: Inflammation Research - December 22, 2022 Category: Research Source Type: research

USP7 accelerates FMR1-mediated ferroptosis by facilitating TBK1 ubiquitination and DNMT1 deubiquitination after renal ischemia –reperfusion injury
ConclusionsUSP7 inhibition attenuated I/R-induced renal injury by inhibiting ferroptosis through decreasing ubiquitination of TBK1 and promoting DNMT1-mediated methylation of FMR1.
Source: Inflammation Research - October 20, 2022 Category: Research Source Type: research

RPL38 knockdown inhibits the inflammation and apoptosis in chondrocytes through regulating METTL3-mediated SOCS2 m6A modification in osteoarthritis
ConclusionRPL38 knockdown inhibited osteoarthritic chondrocyte dysfunction and alleviated OA progression through promoting METTL3-m6A-mediated SOCS2 expression.
Source: Inflammation Research - May 21, 2022 Category: Research Source Type: research

A20 attenuates pyroptosis and apoptosis in nucleus pulposus cells via promoting mitophagy and stabilizing mitochondrial dynamics
ConclusionsTo  sum up, A20 attenuates pyroptosis and apoptosis of NP cells via promoting mitophagy and stabilizing mitochondrial dynamics. Besides, A20 reduces LPS-induced NP cell apoptosis by inhibiting NLRP3 inflammasome-mediated pyroptosis. It provides theoretical support for the reduction of functional NP c ell loss in the intervertebral disc through the gene-targeted intervention of A20.
Source: Inflammation Research - April 15, 2022 Category: Research Source Type: research

Cavin-1 promotes M2 macrophages/microglia polarization via SOCS3
ConclusionsCavin-1 and SOCS3 are actively involved in the process of M2 macrophages/microglia polarization. As a SOCS3 interacting protein, Cavin-1 can promote M2 macrophages/microglia polarization via SOCS3.
Source: Inflammation Research - March 11, 2022 Category: Research Source Type: research

FOXO3a regulates lipid accumulation and adipocyte inflammation in adipocytes through autophagy
ConclusionFOXO3a could promote lipid accumulation and inflammation in differentiated 3T3-L1 adipocytes by targeting autophagy. Our results provide a new theoretical basis for FOXO3a to regulate obesity.
Source: Inflammation Research - April 23, 2021 Category: Research Source Type: research

Glycine is a competitive antagonist of the TNF receptor mediating the expression of inflammatory cytokines in 3T3-L1 adipocytes
ConclusionThese findings support the idea that glycine could partially inhibit the binding of TNF- α to its receptor and provide clues about the mechanisms by which glycine inhibits the secretion of pro-inflammatory adipokines in adipocytes through the TNF-α receptor.
Source: Inflammation Research - April 20, 2021 Category: Research Source Type: research

VIP modulates human macrophages phenotype via FPRL1 via activation of RhoA-GTPase and PLC pathways
ConclusionVIP/FPRL1/VPAC/GTP-RhoA-GTPase signaling modulated macrophages phenotype through activation of multiple signaling pathways including ERK1/2, AKT, P38, ROS, cAMP and calcium.
Source: Inflammation Research - January 27, 2021 Category: Research Source Type: research

microRNA-155-3p attenuates intervertebral disc degeneration via inhibition of KDM3A and HIF1 α
ConclusionThe study concludes that up-regulated miR-155-3p or silenced KDM3A promotes the proliferation, autophagy, and restrains the apoptosis of NP cells of IDD via inhibition of HIF1 α, which may be a promising approach for the treatment of IDD.
Source: Inflammation Research - January 23, 2021 Category: Research Source Type: research

MicroRNA-199-3p up-regulation enhances chondrocyte proliferation and inhibits apoptosis in knee osteoarthritis via DNMT3A repression
ConclusionThis study highlights that miR-199-3p up-regulation or down-regulation of DNMT3A induces chondrocyte proliferation and inhibits apoptosis in KOA, which may widen our eyes to treat patients with KOA.
Source: Inflammation Research - January 12, 2021 Category: Research Source Type: research

TAB1 regulates glycolysis and activation of macrophages in diabetic nephropathy
ConclusionsOur results suggest that the TAB1/NF- κB/HIF-1α signaling pathway regulates glycolysis and activation of macrophages in DN.
Source: Inflammation Research - October 12, 2020 Category: Research Source Type: research

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