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.| File | Dimensione | Formato | |
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TIPS.pdf
Open Access dal 02/10/2023
Descrizione: GPR35, ally of the anti-ischemic ATPIF1-ATP synthase interaction
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