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.

Nesci, S. (2022). GPR35, ally of the anti-ischemic ATPIF1-ATP synthase interaction. TRENDS IN PHARMACOLOGICAL SCIENCES, 43(11), 891-893 [10.1016/j.tips.2022.09.003].

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

Nesci, Salvatore
Primo
Writing – Original Draft Preparation
2022

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.
2022
Nesci, S. (2022). GPR35, ally of the anti-ischemic ATPIF1-ATP synthase interaction. TRENDS IN PHARMACOLOGICAL SCIENCES, 43(11), 891-893 [10.1016/j.tips.2022.09.003].
Nesci, Salvatore
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Descrizione: GPR35, ally of the anti-ischemic ATPIF1-ATP synthase interaction
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11585/896023
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