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. 2018 Jan 26;8:1679. doi: 10.1038/s41598-018-19828-7

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© The Author(s) 2018

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Schematic model for the role of Gbp1 in macrophages. Gbp1 expression is upregulated in response to the stimulation of pro-inflammatory cytokines (IFNγ and LPS) as a defensive mechanism during infection and inflammation. Gbp1 functions in eliminating dysfunctional mitochondria induced during inflammation via promoting mitophagic pathway. During chronic metabolic stress, such as HFD feeding and aging, Gbp1 is downregulated leading to mitochondrial dysfunction and subsequent activation of AMPK-p53 pathway and cellular senescence. Activation of p53 can also limit glycolytic activity of senescent cells.