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

. 2022 Jul 14;19:183. doi: 10.1186/s12974-022-02547-2

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

© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

PMC Copyright notice

Fig. 3 — Molecular signaling pathway of pyroptosis in diabetic retinopathy. A Retinal microvascular endothelial cell (RMEC): increased extracellular ATP binds to P2X7R then activates NLRP3 inflammasome by causing K⁺ efflux and Ca²⁺ influx. TXNIP expression is induced through increased intracellular Ca²⁺ level, miR-590-3p/NOX4/ROS/TXNIP axis, or miR-20b-3p downregulation. After activation, the TXNIP shuttles to mitochondria, competes with apoptosis signal-regulating kinase 1 (ASK1), binds to NLRP3 and activates it; miR-590-3p also targets NLRP1. HG suppresses the voltage-dependent anion channel (VDAC1) expression, causing VDAC1/PINK1/Parkin-mediated mitophagy inhibition. Damaged mitochondria and mtROS accumulation results from impaired mitophagy-activated NLRP3 inflammasome. B Retinal pigment epithelium: hyperglycemia triggers the connexin43/ATP/P2X7R/Ca²⁺ influx pathway, mitochondrial ROS, miR-130a/TNF-α/SOD1/ROS pathway, or METTL3/miR-25-3p/PTEN/Akt/NLRP3 signaling cascade to activate NLRP3 inflammasome. C Pericyte: increased lncRNA MIAT competes with CASP1 mRNA for binding to miR-342-3p, blocking the CASP1 translation and CASP1-dependent pyroptosis. D Microglia (M1): MiR-30a downregulates NLRP3 expression. E Müller cell: hyperglycemia triggers the ROS/TXNIP axis to activate NLRP3 and downregulates the transcription factor nuclear receptor subfamily 4 group A member 2 (Nurr1) to suppress NLRP3 activation