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
Increasing evidence indicates that chronic, low-grade inflammation is a significant contributor to the fundamental pathogenesis of type 2 diabetes mellitus (T2DM). Efferocytosis, an effective way to eliminate apoptotic cells (ACs), plays a critical role in inflammation resolution. Massive accumulation of ACs and the proliferation of persistent inflammation caused by defective efferocytosis have been proven to be closely associated with pancreatic islet β cell destruction, adipose tissue inflammation, skeletal muscle dysfunction, and liver metabolism abnormalities, which together are considered the most fundamental pathological mechanism underlying T2DM. Therefore, here we outline the association between the molecular mechanisms of efferocytosis in glucose homeostasis, T2DM, and its complications, and we analyzed the present constraints and potential future prospects for therapeutic targets in T2DM and its complications.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10335275 | PMC |
http://dx.doi.org/10.2147/JIR.S418334 | DOI Listing |
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