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 constitute the primary barrier within the vessel wall, exhibiting the capacity for angiogenesis, a process implicated in revascularisation.Endothelial cell-mediated angiogenesis is further recognised as a pivotal pathological factor in tumours, pulmonary hypertension, and ocular diseases. Pyruvate kinase type M2 (PKM2) represents a pivotal enzyme in glycolysis, exerting a role in the pathogenic process of diverse diseases through metabolic processes and the transcriptional regulation of key genes. This study established a correlation between PKM2 and angiogenesis in tumours, with the knockdown of PKM2 inhibiting proliferation, migration and angiogenesis in endothelial cells and the over-expression of PKM2 promoting it. Further studies identified ANGPT2 as a downstream target of PKM2, and the supplementation of endothelial cells with ANGPT2 restored proliferation, migration and angiogenesis inhibited by knockdown of PKM2. Collectively, these findings imply that ANGPT2 contributes significantly to the regulation of PKM2-mediated proliferation, migration and angiogenesis.
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Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12381296 | PMC |
http://dx.doi.org/10.1038/s41598-025-17147-2 | DOI Listing |