Hi1a as a Novel Neuroprotective Agent for Ischemic Stroke by Inhibition of Acid-Sensing Ion Channel 1a

Strokes are the second-leading cause of death worldwide, and the cellular and molecular mechanisms underlying stroke-induced brain damage are still uncertain. The present therapy for acute ischemic stroke is limited to thrombolysis with the recombinant tissue plasminogen activator (rtPA). However, rtPA has a narrow therapeutic timeframe of 3–4.5 h, and only approximately 5% of stroke patients can benefit from rtPA treatment. Neuroprotective agents, such as N-methyl-D-aspartate receptor antagonists, have shown great promise in preclinical studies. However, due to a limited therapeutic time window and/or intolerable side effects, they have failed in clinical trials. Extending the time window and reducing side effects for neuroprotective drugs against strokes are critical for effective therapy for stroke patients. A recent study published in Proceedings of the National Academy of Sciences by Irène R. Chassagnon et al. (2017) indicates that Hi1a, a disulfide-rich spider venom peptide, is a highly neuroprotective agent in both in vitro and in vivo studies against experimental stroke. Hi1a reveals neuroprotection through inhibition of acid-sensing ion channel 1a. Thus, Hi1a might be a promising neuroprotective agent to protect the brain from ischemic injury in humans.