ArticleScientific reports2026
Small-molecule FTO inhibitor MO-I-500 protects C8-B4 microglial cells from erastin-induced ferroptosis.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Ferroptosis is a regulated form of cell death driven by iron-dependent lipid peroxidation and the accumulation of lipid-derived reactive oxygen species (ROS). This process has been implicated in various neurological disorders, highlighting the importance of iron metabolism in brain homeostasis. Emerging evidence suggests that epitranscriptomic regulation, particularly N6-methyladenosine (m6A) RNA methylation, may influence ferroptotic signaling pathways. The fat mass and obesity-associated protein (FTO), an m6A RNA demethylase, has been implicated in cellular stress responses; however, its role in ferroptosis remains unclear. Here, we show that inhibition of FTO activity attenuates erastin-induced ferroptosis in C8-B4 microglial cells. Treatment with MO-I-500, a well-characterized FTO inhibitor, significantly decreased erastin-induced cell migration, ROS production, and lipid accumulation. Together, these findings demonstrate that FTO-mediated m6A RNA demethylation plays a crucial role in regulating ferroptotic cell death and suggest that targeting FTO may represent a novel therapeutic strategy for ferroptosis-related neurological disorders.
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