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
Accumulating evidence showed that competing endogenous RNA (ceRNA) mechanism plays a pivotal role in salt sensitivity of blood pressure (SSBP). We constructed a ceRNA network based on SSBP-related differently expressed lncRNAs (2), mRNAs (73) and miRNAs (18). Bioinformatic analyses were utilized to analyze network and found network genes participate in biological pathways related to SSBP pathogenesis such as regulation of nitric oxide biosynthetic process (GO:0045,428) and cellular response to cytokine stimulus (GO:0071,345). Fourteen candidate ceRNA pathways were selected from network to perform RT-PCR validation and found nine RNAs (KCNQ1OT1, SLC8A1-AS1, , , , , , hsa-miR-362-5p and hsa-miR-423-5p) differently expressed between salt-sensitive (SS) and salt-resistant (SR) groups ( < 0.05). Four ceRNA pathways were further validated by luciferase reporter assay and found KCNQ1OT1→hsa-miR-362-5p/hsa-miR-423-5p→ pathways may influence the pathogenic mechanism of SS. Our findings suggested the ceRNA pathway and network may affect SS occurrence mainly through endothelial dysfunction and inflammatory activation.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10731005 | PMC |
http://dx.doi.org/10.1016/j.heliyon.2023.e22466 | DOI Listing |
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