5-HT1F receptor agonism induces mitochondrial biogenesis and increases cellular function in brain microvascular endothelial cells

The study investigates how stimulating the 5-HT1F receptor affects brain microvascular endothelial cells, which are crucial for the blood-brain barrier. These cells were treated with lasmiditan, a drug known to activate this receptor. Researchers found that lasmiditan promotes mitochondrial biogenesis, the creation of new mitochondria, within these cells. It also enhances endothelial cell migration and tube formation, which are important for the development of new blood vessels. The study suggests that activating the 5-HT1F receptor with drugs like lasmiditan could be a promising therapeutic approach for conditions involving mitochondrial and vascular dysfunction in the brain.

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  Lasmiditan treatment increased the maximal oxygen consumption rate, mitochondrial proteins and mitochondrial density in mBMEC, indicative of MB induction.
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  Lasmiditan also enhanced endothelial cell migration and tube formation, key components of angiogenesis.
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  Lasmiditan treatment decreased phosphorylated VE-Cadherin and induced activation of the Akt-FoxO1 pathway, which decreases FoxO1-mediated inhibition of claudin-5 transcription.