GPR35, ally of the anti-ischemic ATPIF1-ATP synthase interaction

Salvatore Nesci

doi:10.1016/j.tips.2022.09.003

GPR35, ally of the anti-ischemic ATPIF1-ATP synthase interaction

Trends Pharmacol Sci. 2022 Nov;43(11):891-893. doi: 10.1016/j.tips.2022.09.003. Epub 2022 Oct 1.

Author

Salvatore Nesci¹

Affiliation

¹ Department of Veterinary Medical Sciences, University of Bologna, Via Tolara di Sopra, 50 - 40064 Ozzano Emilia, Bologna, Italy. Electronic address: salvatore.nesci@unibo.it.

PMID: 36195494
DOI: 10.1016/j.tips.2022.09.003

Abstract

Mitochondrial ATP synthase synthesizes ATP for cellular functions; however, under various conditions, including ischemia, it hydrolyzes ATP, primarily to re-energize the mitochondria. ATP synthase inhibitory factor 1 (ATPIF1) inhibits hydrolysis of ATP by ATP synthase. Wyant and colleagues recently demonstrated that G-protein-coupled receptor 35 (GPR35) is involved in this process. This finding provides an additional framework for the novel discovery of potential therapeutic molecules against ischemia/reperfusion (I/R) injury.

Keywords: ATP inhibitory factor 1; ATP synthase; G-protein-coupled receptor 35; anti-ischemic interaction; kynurenic acid; mitochondria.

Publication types

Comment

MeSH terms

Adenosine Triphosphate
Humans
Ischemia
Mitochondria
Mitochondrial Proton-Translocating ATPases*
Receptors, G-Protein-Coupled
Reperfusion Injury*

Substances

GPR35 protein, human
Receptors, G-Protein-Coupled
Adenosine Triphosphate
Mitochondrial Proton-Translocating ATPases