Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3122
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
Till now, no functional studies for FGF-16 in diabetic heart have been reported. Therefore, this study aims to evaluate the potential function of FGF-16 in inhibiting adverse cardiac remodeling in post myocardial infarction (MI) of diabetic heart. We investigated the role of fibroblast growth factor-16 (FGF-16) in post-MI remodeling and role of cardio-protection in the diabetic infarct heart. Adult db/db diabetic mice were assigned to sham group, MI group and MI+FGF-16 group, respectively. MI group was induced by permanent coronary artery ligation, and the mice were subjected to 2D trans-thoracic echocardiography 2-4 weeks post-surgery. The results showed that the infiltration of monocytes, the associated pro-inflammatory cytokines were significantly increased, and the adverse cardiac remodeling and left ventricular dysfunction were observed in MI group. FGF-16 treatment protected against apoptosis, cardiac dysfunction and chamber dilatation post-MI, and decreased monocyte infiltration and cardiomyocyte hypertrophy/apoptosis. Meanwhile, the FGF-16 treatment also attenuated interstitial fibrosis and myocardial inflammation post-MI, increased M2 macrophage differentiation and associated anti-inflammatory cytokines, reduced adverse remodeling, and improved cardiac function. In conclusion, our results suggest that the heart appears to be a target of systemic and possibly locally generated FGF-16, which plays a therapeutic role in cardiac protection in the post-MI diabetic heart.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5411913 | PMC |
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