Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2021 Jul 12;14:3145–3169. doi: 10.2147/JIR.S310990

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2021 Luo et al.

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).

PMC Copyright notice

The specific pathways of myocardial injury and cardiac dysfunction caused by inflammation-related factors. DAMPs and PAMPs such as HMGB1, ATP and endotoxin from the pancreas and intestine act on membrane receptors such as TLR and P2X7R to recruit inflammatory cells (macrophages, neutrophils and dendritic cells) in serum, activate classical inflammatory pathways such as NF-κB and NLRP3 inflammasome in inflammatory cells, release a large number of pro-inflammatory cytokines, and form a cascade reaction (upper). These inflammatory factors eventually act on cardiomyocytes, causing myocardial energy metabolism disorder, systolic myocardial dysfunction, myocardial hypertrophy, apoptosis and fibrosis through a complex network of signaling pathways (lower).