Matches in SemOpenAlex for { <https://semopenalex.org/work/W2393059332> ?p ?o ?g. }
- W2393059332 abstract "T helper 1 (Th1) type cytokines and chemokines are bioactive mediators in inflammation underling several diseases and co-morbid conditions, such as cardiovascular and metabolic disorders. Th1 chemokine CXCL10 participates in heart damage initiation/progression; cardioprotection has been recently associated with sildenafil, a type 5 phosphodiesterase inhibitor. We aimed to evaluate the effect of sildenafil on CXCL10 in inflammatory conditions associated with diabetic cardiomyopathy. We analyzed: CXCL10 gene and protein in human cardiac, endothelial, and immune cells challenged by pro-inflammatory stimuli with and without sildenafil; serum CXCL10 in diabetic subjects at cardiomyopathy onset, before and after 3 months of treatment with sildenafil vs. placebo. Sildenafil significantly decreased CXCL10 protein secretion (IC50 = 2.6 × 10(-7)) and gene expression in human cardiomyocytes and significantly decreased circulating CXCL10 in subjects with chemokine basal level ≥ 930 pg/ml, the cut-off value as assessed by ROC analysis. In conclusion, sildenafil could be a pharmacologic tool to control CXCL10-associated inflammation in diabetic cardiomyopathy." @default.
- W2393059332 created "2016-06-24" @default.
- W2393059332 creator A5006150148 @default.
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- W2393059332 creator A5083248311 @default.
- W2393059332 date "2016-05-10" @default.
- W2393059332 modified "2023-09-27" @default.
- W2393059332 title "Phosphodiesterase Type 5 Inhibitor Sildenafil Decreases the Proinflammatory Chemokine CXCL10 in Human Cardiomyocytes and in Subjects with Diabetic Cardiomyopathy" @default.
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- W2393059332 doi "https://doi.org/10.1007/s10753-016-0359-6" @default.
- W2393059332 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4883282" @default.
- W2393059332 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27165639" @default.