Relevance and application of sirtuin 3-activated mitophagy in gastric cancer treatment

Sirtuin 3 (SIRT3) is a primary mitochondrial deacetylase. Studies have confirmed that it directly activates mitophagy by modulating mitochondrial protein acetylation. As a key homeostatic mechanism, mitophagy activation alleviates oxidative stress-induced imbalance between cell proliferation and apoptosis, corrects stress-driven mitochondrial metabolic dysfunction, and thus inhibits excessive tumor growth, exerting significant antitumor effects. These functions establish SIRT3 as a key target for regulating mitophagy and cancer therapy. Clinically, strategies centered on its precise regulation may offer a novel direction for gastric cancer (GC) prevention and treatment, with selective activation remaining a critical challenge. SIRT3 could also serve as an auxiliary indicator in clinical guidelines for assessing tumor progression. Given this potential, this mini-review systematically examines SIRT3's mechanisms in regulating mitophagy, its role in GC pathogenesis, and translational prospects for targeting SIRT3 in GC management.