Calpain as a Therapeutic Target for Hypoxic-Ischemic Encephalopathy

Hypoxic-ischemic encephalopathy (HIE) is a complex pathophysiological process with multiple links and factors. It involves the interaction of inflammation, oxidative stress, and glucose metabolism, and results in acute and even long-term brain damage and impairment of brain function. Calpain is a family of Ca2+-dependent cysteine proteases that regulate cellular function. Calpain activation is involved in cerebral ischemic injury, and this involvement is achieved by the interaction among Ca2+, substrates, organelles, and multiple proteases in the neuronal necrosis and apoptosis pathways after cerebral ischemia. Many calpain inhibitors have been developed and tested in the biochemical and biomedical fields. This study reviewed the potential role of calpain in the treatment of HIE and related mechanism, providing new insights for future research on HIE.

Automated summary

Hypoxic-ischemic encephalopathy (HIE) is a complex process involving inflammation, oxidative stress, and glucose metabolism, leading to brain damage and impairment. Calpain, a family of Ca2+-dependent cysteine proteases, is involved in cerebral ischemic injury and plays a role in neuronal necrosis and apoptosis pathways. This study reviews the potential role of calpain in treating HIE and provides insights for future research.