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
Chronic kidney disease (CKD) is associated with an increased risk of death from cardiovascular disease (CVD). One factor involved in CVD development is nitric oxide (NO), which acts as a powerful vasodilator. NO is produced via the nitrogen cycle, through the reduction of nitrate to nitrite with the process mainly occurring in the mouth by commensal microbiota. People with CKD have compromised microbiota (dysbiosis) with an increased abundance of potentially pathogenic and pro-inflammatory bacteria capable of producing uremic toxins that contribute to CKD development and reduce enzymatic NO production. However, to date, few studies have comprehensively documented the gut or saliva microbiota in the CKD population or investigated the role of NO in people with CKD. This review will discuss NO pathways that are linked to the progression of CKD and CVD and therapeutic options for targeting these pathways.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1016/j.niox.2016.05.002 | DOI Listing |
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