Review reveals nanomaterial strategies for bidirectional ferroptosis control across cancer and inflammatory conditions, highlighting avenues for precision nanomedicine.
Key Points
Synthesize rational nanomaterial design principles for modulating ferroptotic cell death pathways across both oncological and non-cancer disease contexts.
Reviewed molecular mechanisms driving iron-dependent ferroptotic cell death and identified regulatory checkpoints.
Evaluated physicochemical and structural designs of nanoplatforms engineered to either promote ferroptosis in malignant cells or inhibit it in non-cancer pathologies.
Nanomaterial systems overcome small-molecule limitations by improving cell-specific delivery, pharmacokinetic half-life, and spatiotemporal responsiveness.
Dual-function nanoplatforms achieve targeted tumor suppression via ferroptosis induction while effectively dampening ferroptosis to preserve tissue in neurodegenerative, inflammatory, and metabolic diseases.