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
98%
921
2 minutes
20
Anti-cancer therapy offers significant risks for cardiovascular diseases, including hypertension, thromboembolic ischaemia, arrhythmias, dyslipidaemia, hyperglycemia, obesity, and high cholesterol. Cardiotoxicity is a leading cause of elevated mortality rates among cancer patients, and anti-cancer drugs often contribute to this issue. Emerging research highlights the role of microRNA (miRNAs) in regulating drug-induced cardiotoxicity by influencing genetic, epigenetic, transcriptional, and translational processes. MiRNAs have potential as biomarkers for early detection and treatment. Moreover, novel diagnostic and therapeutic approaches targeting miRNAs could improve the clinical management of cardiotoxicity in cancer patients. This study is based on regulatory mechanisms behind cardiotoxicity, including oxidative stress, vascular homeostasis, mitochondrial damage, apoptosis, and inflammation, and explores strategies for managing these complications in cancer therapy.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.2174/0109298673386907250730010201 | DOI Listing |