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: 1075
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3195
Function: GetPubMedArticleOutput_2016
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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Myocardial infarction (MI) poses a significant threat to human health. Current treatments emphasize early revascularization to restore blood supply to the myocardium, often overlooking the extensive oxidative damage and autophagy dysfunction resulting from reactive oxygen species (ROS) release after MI. Therefore, timely and effective interventions to clear ROS in the early stages of MI are crucial for inhibiting the MI pathological progression and restoring cardiac function. This study constructed a ROS-responsive biomimetic nanoparticle (PNP@NbC-MSN) by integrating niobium carbide MXenes (NbC) onto mesoporous silica nanoparticle (MSN) coated with platelet membrane. During the MI acute phase, these nanoparticles are targeted and delivered to the infarcted heart via intravenous injection. The MSN mesoporous structure enhances the ROS scavenging capacity of NbC, eliminating excess ROS in the infarct region and inhibiting the oxidative stress progression. Silicon ions released from MSN further promote angiogenesis within the infarct region. PNP@NbC-MSN reduces inflammation by downregulating the NF-κB pathway and enhances autophagy by activating the AMPK pathway, thereby blocking pathological microenvironmental progression after MI and improving cardiac function. In vitro and in vivo results highlight the therapeutic potential of PNP@NbC-MSN in MI, offering a promising MI treatment strategy.
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Source |
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http://dx.doi.org/10.1002/adhm.202404979 | DOI Listing |