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
Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal disease without therapeutic options. The development of new therapeutic strategies for the disease is needed. IPF is characterized by myofibroblast accumulation and collagen overproduction. Transforming growth factor-β1 (TGF-β1) is a key cytokine activating these pathological processes. Heat shock proteins (HSPs) are crucial regulators and promote TGF-β1 activity. Among them, HSP27 is overexpressed in animal models and in the lung of patients with IPF. HSP27 activates pro-fibrotic mechanisms and therefore may represents a potential target. Strategies aiming to inhibit HSP27 might pave the way towards new treatment options for patients with IPF.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1016/j.rmr.2020.02.007 | DOI Listing |
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