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
Traumatic brain injury (TBI) is a worldwide health problem contributing to significant economic burden. TBI is difficult to treat partly due to incomplete understanding of pathophysiology. Ferroptosis is a type of iron-dependent programmed cell death which has gained increasing attention due to its possible role in TBI. Current studies have demonstrated that ferroptosis is related to the pathology of TBI, and inhibition of ferroptosis may improve long term outcomes of TBI. Therefore, clarification of the exact association between ferroptosis and traumatic brain injury is necessary and may provide new targets for treatment. This review describes (1) the ferroptosis pathways following traumatic brain injury, (2) the role of ferroptosis during the chronic phase of traumatic brain injury, and (3) potential therapies targeting the ferroptosis pathways.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1016/j.brainresbull.2021.04.023 | DOI Listing |
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