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

. 2016 Oct 13;2:16022. doi: 10.1038/npjamd.2016.22

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

Copyright © 2016 The Author(s)

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

PMC Copyright notice

Increased fatty acid oxidation (FAO) is a beneficial adaptive response to genotoxic stress. (a) Relative MDF cell number 24 h after 20 Jm/² UV-C and/or 40 μM Etomoxir treatment (n=2 independent MDF lines/genotype in duplicate); Student’s t-test between indicated groups. (b) Relative cell number of WT and AMPKα1KO MDFs 24 h after ultraviolet (UV)-C or mitomycin C (MMC; n=2 MDF lines/genotype in duplicate); Student’s t-test versus untreated within genotype and treatment. *P<0.05, **P<0.01. (c) Kaplan–Meier survival plots of CX mice on methionine restricted (MetR; n=17) or methionine complete (MetC; n=8) diets; log-rank test P=0.0004. (d) Model of relationship between DNA damage and maintenance of cellular and organismal energy homeostasis. Acute and chronic genotoxic stress activate PARP-1, depleting steady-state ATP and NAD+ levels, activating AMPK and increasing FAO/OXPHOS to restore energy homeostasis.