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

. 2024 Feb 29;11:1305431. doi: 10.3389/fmed.2024.1305431

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

Copyright © 2024 Wang, Zhang, Shen, Wei, Zhao, Xiao, Lv, Qin, Xu, Zhou, Xie, Li and Xie.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Gouty nephropathy (GN) cell apoptosis. Tumor necrosis factor receptor (TNFR) and factor-associated apoptosis (Fas) receptors induce apoptosis by binding to their respective ligands and cleaving Pro-Caspase-8 through the death domains TNF-associated death domain (TRADD) and Fas-associated death domain (FADD), producing active caspase-8 and activating caspase-3, triggering apoptosis. MSU causes oxidative stress and impairs mitochondrial function, leading to the release of the pro-apoptotic factor Bcl-2 (B-cell lymphoma-2), activating the P53 transcription factor, promoting caspase-9 and caspase-3, and ultimately triggering apoptosis.