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 Jan 13;11:968. doi: 10.1038/s41598-020-80244-x

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

© The Author(s) 2021

Open Access This 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/.

PMC Copyright notice

Proposed model for A2AR activation and activation of autophagy. CGS21680 or adenosine binds the A2AR, a Gs-associated GPCR which signals via cAMP to activate PKA or EPAC1/2 (not shown) leading to activation of downstream signaling culminating in nuclear transport and activation of FoxO1/3. There is also nearly simultaneous export of initially nuclearly-located inactive AKT-phosphorylated FoxO1/3 that exits the nucleus on its way to proteosomal degradation. Active FoxO1/3 are known to lead to up-regulation of autophagy genes in addition to participation in other homeostatic pathways as listed in the box on the left. These processes lead to a reduction of OA with improved health of articular cartilage.