Protective succinate-SUCNR1 metabolic stress signaling gone bad

Sally Winther; Mette Trauelsen; Thue W Schwartz

doi:10.1016/j.cmet.2021.06.009

Protective succinate-SUCNR1 metabolic stress signaling gone bad

Cell Metab. 2021 Jul 6;33(7):1276-1278. doi: 10.1016/j.cmet.2021.06.009.

Authors

Sally Winther¹, Mette Trauelsen¹, Thue W Schwartz²

Affiliations

¹ The Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Panum Institute, Mærsk Tower 07.6, Blegdamsvej 3B, Copenhagen, Denmark.
² The Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Panum Institute, Mærsk Tower 07.6, Blegdamsvej 3B, Copenhagen, Denmark. Electronic address: tws@sund.ku.dk.

PMID: 34233171
DOI: 10.1016/j.cmet.2021.06.009

Abstract

The TCA cycle metabolite succinate functions as an intra- and extracellular signal of metabolic stress. Based on the phenotype of UCP-1-deficient mice, Mills et al. (2021) now report in Nature Metabolism that accumulation of extracellular succinate due to impaired elimination in thermogenic fat drives liver inflammation and fibrosis through the succinate receptor SUCNR1.

Publication types

Research Support, Non-U.S. Gov't
Comment

MeSH terms

Animals
Fibrosis
Mice
Receptors, G-Protein-Coupled*
Signal Transduction
Stress, Physiological
Succinic Acid*

Substances

Receptors, G-Protein-Coupled
Succinic Acid