Severity: Warning
Message: file_get_contents(https://...@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 197
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 197
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 271
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3165
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 597
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 511
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 317
Function: require_once
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Endothelial cells (ECs) integrate immune and vascular functions to promote host defense against pathogens. While previously studied as forming passive flow conduits, ECs are now recognized as active contributors to maladaptive inflammation. During acute infection, ECs may promote tissue pathologies, including hypoxia, acidosis, electrolyte disturbances, and capillary barrier breakdown. These pathologies significantly contribute to organ dysfunction and septic shock. In chronic vascular infection, ECs may promote loss of vascular quiescence, contributing to vascular malformations and vaso-occlusive lesions. In this review, we discuss the interplay between the immune and vascular roles of blood ECs, an emerging area of interest with therapeutic implications. While previously overlooked, therapies targeting dysregulation of EC function(s) may show clinical benefit towards improving outcomes related to both acute and chronic forms of infection.
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http://dx.doi.org/10.1016/j.coi.2025.102648 | DOI Listing |