Manoalide se dirige a la vulnerabilidad redox-mitocondrial para inducir el fallo bioenergético y suprimir la actividad angiogénica en glioblastoma

moiety of manoalide, which may contribute to its redox-modulating properties. In addition to tumor cell-intrinsic effects, manoalide suppressed endothelial migration, tube formation, and microvessel sprouting, suggesting anti-angiogenic activity in complementary endothelial and ex vivo angiogenesis models. Collectively, our findings integrate PLA2G4A-based transcriptomic evidence with functional analyses, suggesting manoalide-mediated disruption of mitochondrial redox homeostasis may represent a potential strategy to induce bioenergetic dysfunction, apoptosis-associated signaling, autophagy-associated stress