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
Despite the significant alleviation of clinical cardiovascular diseases through appropriate interventional treatments, the recurrence of vascular restenosis necessitating reoperation remains a substantial challenge impacting patient prognosis. Plant-derived exosome-like nanovesicles (PELNs) are integral to interspecies cellular communication, with their functions and potential applications garnering significant attention from the research community. This study extracted -derived exosome-like nanovesicles (SL-ELNs) and demonstrated their inhibition of PDGF-BB-induced proliferation, migration, and phenotypic transformation of vascular smooth muscle cells (VSMCs). Mechanistically, miRNA164a/b-5p within the SL-ELNs reduced the expression of Keap1 mRNA, thereby increasing nuclear translocation of Nrf2 and enhancing the expression of antioxidant genes to alleviate oxidative stress. In a mouse carotid artery injury model, it was further confirmed that miRNA164a/b-5p within the SL-ELNs could inhibit neointimal hyperplasia. These results suggest that SL-ELNs inhibit VSMCs proliferation, migration, and phenotypic transformation, and they might be potential therapeutic agents for the prevention or treatment of restenosis.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1039/d4fo03993a | DOI Listing |
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