Liraglutide protects high-glucose-stimulated fibroblasts by activating the CD36-JNK-AP1 pathway to downregulate P4HA1
Biomedicine & Pharmacotherapy, ISSN: 0753-3322, Vol: 118, Page: 109224
2019
- 26Citations
- 22Captures
Metric Options: CountsSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations26
- Citation Indexes26
- 26
- CrossRef17
- Captures22
- Readers22
- 22
Article Description
Diabetic cardiomyopathy (DCM) is a serious complication of diabetes mellitus. It’s known that glucagon-like peptide-1 (GLP-1) and prolyl 4-hydroxylase subunit alpha-1 (P4HA1) have significant effect on cardiovascular function, but their interaction in cardiac fibroblasts (CFs) is still being unraveled. The present study demonstrated that glucose promotes CFs proliferation and cardiac fibrosis. Using qRT-PCR, Western blot, CCK-8, EdU, flow cytometry, wound healing and Transwell assays to explore the functions of liraglutide and P4HA1 in high-glucose (HG)-induced CFs, we proved that liraglutide as well as silencing of P4HA1 inhibited cell proliferation, migration and invasion, and promoted cell cycle arrest and apoptosis in HG-induced CFs. In addition, liraglutide downregulated P4HA1 expression, upregulated CD36 and P-JNK expression levels, and enhanced the DNA binding activity of AP-1 on P4HA1. Inhibition of CD36 or p--JNK promoted P4HA1 expression. Liraglutide may down-regulate P4HA1 expression at least partly though CD36-JNK-AP1 pathway, thereby reducing myocardial fibrosis. Therefore, our study provides novel insight into the molecular mechanism and function of liraglutide in HG-mediated CFs.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0753332219311138; http://dx.doi.org/10.1016/j.biopha.2019.109224; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85069671400&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/31349139; https://linkinghub.elsevier.com/retrieve/pii/S0753332219311138; https://dx.doi.org/10.1016/j.biopha.2019.109224
Elsevier BV
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