Distinct molecular pathways of cell death drive the progression of neurological pathologies. Targeting the signaling cascades induced by oxidative stress and inflammation within these pathways is central to developing cytoprotective therapies against apoptosis, ferroptosis, and excitotoxicity. In recent years, the flavonoid icariin has emerged as a promising candidate, showing significant potential to intercept these specific cell death mechanisms. However, while the current literature highlights icariin’s general neuroprotective effects, evidence regarding its precise interaction with distinct cell death modalities remains fragmented. This review synthesizes current knowledge to clarify the molecular logic by which icariin modulates these specific pathways in neurological models.
Rodrigues-Soares et al. (Fri,) studied this question.