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: 1034
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3152
Function: GetPubMedArticleOutput_2016
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
Purpose Of Review: In recent years, a family of adiponectin paralogs designated as C1q/TNF-related protein (CTRP) has attracted increasing attention. They are inflammatory adipocytokines mostly secreted from epicardial adipose tissue, which modulate the development and prognosis of coronary artery disease (CAD). This review summarizes the pathophysiological roles of individual members of the CTRP superfamily in the development of CAD.
Recent Findings: Recent studies have revealed how members of the CTRP family, CTRP1, CTRP3, CTRP5, CTRP9, CTRP12, and CTRP13, can influence both development and progression of CAD by modulating metabolic pathways, influencing immuno-inflammatory response, and regulating cardiovascular functions. Research to date has not been sufficient to answer the specific mechanism of the CTRP family in the occurrence and development of CAD. This review explores the evidence of CTRP superfamily regulating different pathophysiology stages of CAD through the immuno-inflammation, glucose and lipid metabolism, and vascular endothelial function.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7256102 | PMC |
http://dx.doi.org/10.1007/s11883-020-00840-0 | DOI Listing |
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