Lasmiditan promotes recovery from acute kidney injury through induction of mitochondrial biogenesis

Abstract

AKI pathology involves a rapid decline in kidney function and occurs in 8–16% of hospitalized patients. There is currently no therapeutic for AKI. AKI results in mitochondria dysfunction, microvasculature injury, and loss of renal tubular function. In an I/R-induced AKI mouse model, treatment with the FDA-approved 5-HT1F receptor-selective agonist lasmiditan induced mitochondrial biogenesis, improved vascular integrity, reduced fibrosis, and reduced proximal tubule damage. These data support repurposing lasmiditan for the treatment of AKI.