Results 21 to 30 of about 1,817 (168)

Bioinformatic analysis identifies GPR91 as a potential key gene in brain injury after deep hypothermic low flow

open access: yesHeliyon, 2023
Purpose: Explore the transcription change of brain ischemia and reperfusion injury after deep hypothermic low flow. Method: The data from PRJNA739516 and GSE104036 were obtained for the differentially expressed genes identification, functional enrichment
Song Puwei   +7 more
doaj   +2 more sources

G-Protein-Coupled Receptor 91-Dependent Signalling Does Not Influence Vascular Inflammation and Atherosclerosis in Hyperlipidaemic Mice [PDF]

open access: yesCells, 2023
The TCA cycle intermediate metabolite ‘succinate’ has been proposed as an inflammatory mediator, influencing autoimmunity and allergic reactions, through ligation to its sensing receptor SUCNR1/GPR91.
Silke Griepke   +6 more
doaj   +2 more sources

Transcription factors regulate GPR91-mediated expression of VEGF in hypoxia-induced retinopathy [PDF]

open access: yesScientific Reports, 2017
AbstractHypoxia is the most important factor in the pathogenesis of diabetic retinopathy (DR). Our previous studies demonstrated that G protein-coupled receptor 91(GPR91) participated in the regulation of vascular endothelial growth factor (VEGF) secretion in DR.
Li, Tingting   +5 more
openaire   +3 more sources

GPR91 Receptor Mediates Protection against Doxorubicin-Induced Cardiotoxicity without Altering Its Anticancer Efficacy. An In Vitro Study on H9C2 Cardiomyoblasts and Breast Cancer-Derived MCF-7 Cells

open access: yesCells, 2020
Doxorubicin (DOX) is an anticancer drug widely used in oncology, especially for breast cancer. The main limitation of DOX treatment is its cardiotoxicity due to the cumulative dose.
Matthieu Dallons   +4 more
doaj   +2 more sources

Extracellular succinate hyperpolarizes M2 macrophages through SUCNR1/GPR91-mediated Gq signaling [PDF]

open access: yesCell Reports, 2021
Summary: Succinate functions both as a classical TCA cycle metabolite and an extracellular metabolic stress signal sensed by the mainly Gi-coupled succinate receptor SUCNR1. In the present study, we characterize and compare effects and signaling pathways
Mette Trauelsen   +11 more
doaj   +5 more sources

Metabolic Memory in Cardiovascular Disease: Encoding, Propagation, and Therapeutic Targeting. [PDF]

open access: yesAdv Sci (Weinh)
Cardiovascular risk often persists after metabolic abnormalities are corrected. This conceptual Review frames such persistence as metabolic memory, encoded through a narrowing therapeutic window from reversible marks to irreversible damage, with continuous input from peripheral organs.
Cheng C   +12 more
europepmc   +2 more sources

The fate of P2Y-related orphan receptors: GPR80/99 and GPR91 are receptors of dicarboxylic acids [PDF]

open access: yesPurinergic Signalling, 2004
Several orphan G protein-coupled receptors are structurally close to the family of P2Y nucleotide receptors: GPR80/99 and GPR91 are close to P2Y(1/2/4/6/11) receptors, whereas GPR87, H963 and GPR34 are close to P2Y(12/13/14). Over the years, several laboratories have attempted without success to identify the ligands of those receptors.
Suarez Gonzalez, Nathalie   +3 more
openaire   +5 more sources

GPR91 senses extracellular succinate released from inflammatory macrophages and exacerbates rheumatoid arthritis [PDF]

open access: yesJournal of Experimental Medicine, 2016
When SUCNR1/GPR91-expressing macrophages are activated by inflammatory signals, they change their metabolism and accumulate succinate. In this study, we show that during this activation, macrophages release succinate into the extracellular milieu.
Amanda Littlewood-Evans   +14 more
openaire   +3 more sources

Deficiency in the metabolite receptor SUCNR1 (GPR91) leads to outer retinal lesions

open access: yesAging, 2013
Age-related macular degeneration (AMD) is a prominent cause of blindness in the Western world. To date, its molecular pathogenesis as well as the sequence of events leading to retinal degeneration remain largely ill-defined. While the invasion of choroidal neovessels in the retina is the primary mechanism that precipitates loss of sight, an earlier dry
Favret   +15 more
openaire   +3 more sources

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