FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4364351840> ?p ?o ?g. }

• W4364351840 abstract "Autonomic imbalance and metabolic inflammation are important pathological processes in diabetic cardiomyopathy. Gut microbiota dysbiosis and increased levels of bacterial component lipopolysaccharide (LPS) are associated with diabetic myocardial injury, but the mechanism by which gut microbes affect metabolic inflammation and cardiac injury remains unclear. We determined whether pyridostigmine (PYR), which inhibits cholinesterase to improve vagal activity, could regulate the disordered gut microbiota and attenuate gut barrier dysfunction, metabolic endotoxemia, and inflammation in diabetes. Db/db mice exhibited high blood glucose levels, insulin resistance, low vagal activity, and diabetic myocardial injury. Db/db mice also exhibited gut microbiota perturbations and subsequent disruption of gut barrier function, resulting in an influx of LPS, metabolic endotoxemia, and inflammation. PYR ameliorated the dysregulated glucose and lipid metabolism, modulated the overall structure of the gut microbiota, selectively enhanced the abundance of anti-inflammatory bacteria, and reduced the abundance of proinflammatory and potentially pathogenic bacteria in db/db mice. Importantly, PYR enhanced vagal activity, restored gut microbiota homeostasis, and alleviated gut barrier dysfunction. Therefore, the LPS-induced extracellular signal-regulated kinase (ERK)/early growth response-1 (Egr-1) pathway and consequent metabolic inflammation were inhibited, and eventually, cardiac hypertrophy, fibrosis, oxidative stress, and dysfunction were ameliorated in db/db mice. In vitro cardiomyocyte injury was induced by exposing primary neonatal rat ventricular cardiomyocytes to high glucose (HG) and LPS. In vitro analyses showed that HG + LPS induced ERK1/2 phosphorylation, Egr-1 expression, inflammation, and cell apoptosis, which were inhibited by acetylcholine (ACh). Alpha 7 nicotinic ACh receptor but not muscarinic 2 ACh receptor plays an important role in ACh-mediated anti-inflammatory effects and inhibiting the ERK/Egr-1 pathway in HG + LPS-administered neonatal rat ventricular cardiomyocytes. PYR and ACh ameliorated diabetic myocardial injury by inhibiting the LPS-induced ERK/Egr-1 pathway and metabolic inflammation. The vagus-gut-heart axis has provided new insights into the complex mechanisms of diabetes and offers novel therapeutic targets." @default.
• W4364351840 created "2023-04-12" @default.
• W4364351840 creator A5001272873 @default.
• W4364351840 creator A5039341144 @default.
• W4364351840 creator A5069165624 @default.
• W4364351840 creator A5083069101 @default.
• W4364351840 creator A5083157583 @default.
• W4364351840 date "2023-04-11" @default.
• W4364351840 modified "2023-10-11" @default.
• W4364351840 title "Cholinergic drugs reduce metabolic inflammation and diabetic myocardial injury by regulating the gut bacterial component lipopolysaccharide‐induced <scp>ERK</scp>/Egr‐1 pathway" @default.
• W4364351840 cites W1511458250 @default.
• W4364351840 cites W2000694690 @default.
• W4364351840 cites W2002556835 @default.
• W4364351840 cites W2059787600 @default.
• W4364351840 cites W2068111669 @default.
• W4364351840 cites W2069368135 @default.
• W4364351840 cites W2073295417 @default.
• W4364351840 cites W2073514994 @default.
• W4364351840 cites W2097033993 @default.
• W4364351840 cites W2161275684 @default.
• W4364351840 cites W2166739673 @default.
• W4364351840 cites W2298848525 @default.
• W4364351840 cites W2405795356 @default.
• W4364351840 cites W2551150937 @default.
• W4364351840 cites W2567641807 @default.
• W4364351840 cites W2606251550 @default.
• W4364351840 cites W2766947086 @default.
• W4364351840 cites W2782308903 @default.
• W4364351840 cites W2791998898 @default.
• W4364351840 cites W2794419196 @default.
• W4364351840 cites W2801492412 @default.
• W4364351840 cites W2889018234 @default.
• W4364351840 cites W2891072944 @default.
• W4364351840 cites W2909542676 @default.
• W4364351840 cites W2913520142 @default.
• W4364351840 cites W2917446705 @default.
• W4364351840 cites W2949055452 @default.
• W4364351840 cites W2955753510 @default.
• W4364351840 cites W2964615919 @default.
• W4364351840 cites W2965140029 @default.
• W4364351840 cites W2966354475 @default.
• W4364351840 cites W2967632204 @default.
• W4364351840 cites W2971322914 @default.
• W4364351840 cites W2975938102 @default.
• W4364351840 cites W2988933432 @default.
• W4364351840 cites W3000003327 @default.
• W4364351840 cites W3010009645 @default.
• W4364351840 cites W3015139203 @default.
• W4364351840 cites W3045922743 @default.
• W4364351840 cites W3080798241 @default.
• W4364351840 cites W3082866225 @default.
• W4364351840 cites W3089678726 @default.
• W4364351840 cites W3119611628 @default.
• W4364351840 cites W3125156235 @default.
• W4364351840 cites W3133576348 @default.
• W4364351840 cites W3137787607 @default.
• W4364351840 cites W3138774893 @default.
• W4364351840 cites W3139326682 @default.
• W4364351840 cites W3146864616 @default.
• W4364351840 cites W3158133555 @default.
• W4364351840 cites W3161197203 @default.
• W4364351840 cites W3161566328 @default.
• W4364351840 cites W3172891882 @default.
• W4364351840 cites W3174028200 @default.
• W4364351840 cites W3176533716 @default.
• W4364351840 cites W3181820352 @default.
• W4364351840 cites W3211861956 @default.
• W4364351840 cites W4200026682 @default.
• W4364351840 cites W4200215232 @default.
• W4364351840 cites W4210445316 @default.
• W4364351840 cites W4210603076 @default.
• W4364351840 cites W4214700275 @default.
• W4364351840 cites W4280644066 @default.
• W4364351840 cites W4285589601 @default.
• W4364351840 cites W4291285132 @default.
• W4364351840 cites W4293677832 @default.
• W4364351840 cites W4295809293 @default.
• W4364351840 cites W4304194195 @default.
• W4364351840 doi "https://doi.org/10.1096/fj.202202108r" @default.
• W4364351840 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37039813" @default.
• W4364351840 hasPublicationYear "2023" @default.
• W4364351840 type Work @default.
• W4364351840 citedByCount "1" @default.
• W4364351840 countsByYear W43643518402023 @default.
• W4364351840 crossrefType "journal-article" @default.
• W4364351840 hasAuthorship W4364351840A5001272873 @default.
• W4364351840 hasAuthorship W4364351840A5039341144 @default.
• W4364351840 hasAuthorship W4364351840A5069165624 @default.
• W4364351840 hasAuthorship W4364351840A5083069101 @default.
• W4364351840 hasAuthorship W4364351840A5083157583 @default.
• W4364351840 hasConcept C126322002 @default.
• W4364351840 hasConcept C134018914 @default.
• W4364351840 hasConcept C164027704 @default.
• W4364351840 hasConcept C203014093 @default.
• W4364351840 hasConcept C2776914184 @default.
• W4364351840 hasConcept C2778754761 @default.
• W4364351840 hasConcept C539455810 @default.
• W4364351840 hasConcept C71924100 @default.
• W4364351840 hasConcept C86803240 @default.
• W4364351840 hasConceptScore W4364351840C126322002 @default.

• next