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Matyskiela, M.E., Lander, G.C
Acta Ophthalmologica Scandinavica
The elabela-APJ axis could mitigate neuronal ferroptosis following ischemic stroke, and the ELA-32 peptide may be a potential therapeutic candidate for ischemic stroke and cardiovascular diseases
This chronic glucocorticoid excess, in turn, promotes neuronal dysfunction and contributes to the pathogenesis of depressive-like behaviors ( subunits on corticotropin-releasing hormone (CRH) neurons resulted in limited post-seizure corticosterone (CORT) elevation
