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

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

Automated summary

Mitochondrial ATP synthase synthesizes ATP for cellular functions, but it can also hydrolyze ATP under various conditions to re-energize the mitochondria. ATP synthase inhibitory factor 1 (ATPIF1) inhibits this hydrolysis process. Recent research has shown that G-protein-coupled receptor 35 (GPR35) is involved in this process, providing a new framework for the discovery of potential therapeutic molecules against ischemia/reperfusion (I/R) injury.