Calpain in Acute Hepatic Encephalopathy: A Player in Pathophysiology and a Possible Target for Pharmacological Intervention

 Calpain in Acute Hepatic Encephalopathy: A Player in Pathophysiology and a Possible Target for Pharmacological Intervention

Acute hepatic encephalopathy (AHE) is a rapidly worsening neuropsychiatric syndrome, secondary to acute liver failure (ALF). In most cases, AHE is fatal without liver transplantation. Extending the survival of AHE patients is clinically important, hoping to find appropriate livers for transplantation. Neuroprotection and hepatoprotection can offer future prospects to achieve this goal. Ammonia which is increased in the brain of AHE patients stimulates the activity of N-methyl-Daspartatre (NMDA) receptors. Based on animal studies reporting beneficial effects of inhibition of these receptors, we hereby suggest that calpain, a Ca2+ -dependent proteolytic enzyme and a downstream mediator of cell injury conferred by over-stimulation of NMDA receptors, can play role in the pathogenesis of brain injury in AHE.