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 Nov 8;8:737652. doi: 10.3389/fcvm.2021.737652

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

Copyright © 2021 Zhang, Feng, Li, Chen, Ning, Ou and Chen.

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

Mitochondrial homeostasis mediated inflammation of Cd-caused AS in vivo. (A–D) The protein expression levels of RIPK3 and p-MLKL in the ApoE^−/− mice treated with Cd, NAC, and Mdivi-1. (E–G) The protein expression levels of Opa1, Drp1, LC3I, and LC3II in the mitochondria of the aortic arch in the ApoE^−/− mice after the treatment with Cd, high-fat, and Mdivi-1. (H) Aortic arch of the Cd-, high-fat-, NAC-, and Mdivi-1-treated ApoE^−/− mice were probed with specific antibodies against the macrophage marker F4/80 and co-probed with antibodies against the markers of M1 (CD86). (I) Quantification of CD86⁺ of the F4/80⁺ area in the aortic arch. (J,K) The protein expression levels of NLRP3 and pNF-KB in the mice aortic arch (n = 5–7 per group). Data are shown as mean ± SD. ^*p < 0.05, ^**p < 0.01, ^***p < 0.001, ^****p < 0.0001.