ArticleBiochemical pharmacology2023
Lasmiditan restores mitochondrial quality control mechanisms and accelerates renal recovery after ischemia-reperfusion injury.
Article in Biochemical pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Mitophagy in kidney transplantation ischemia-reperfusion injury.International urology and nephrology · 2026Review
- Review
- 5-Hydroxytryptamine 1F receptor loss reduces renal vasculature and prevents lasmiditan-induced recovery following moderate-severe acute kidney injury in mice.American journal of physiology. Renal physiology · 2025Article
- Harnessing mitochondrial biogenesis to combat acute kidney injury: Current insights and futuredirections.Genes & diseases · 2025Review
- MARY1 restores mitochondrial homeostasis and accelerates renal recovery following acute kidney injury.American journal of physiology. Renal physiology · 2025Article
- Mitochondrial Quality Control in Health and Disease.MedComm · 2025Review
- Serotonin regulation of mitochondria in kidney diseases.Pharmacological research · 2024Review
- Mitophagy regulates mitochondrial number following pharmacological induction of mitochondrial biogenesis in renal proximal tubule cells.Frontiers in pharmacology · 2024Article
- Research Hotspots in Mitochondria-Related Studies for AKI Treatment: A Bibliometric Study.Drug design, development and therapy · 2024Article
- 5-HTFrontiers in cellular neuroscience · 2024Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMitochondrial dysfunction is a well-established result of acute kidney injury (AKI). Previously, we identified that 5-hydroxytryptamine 1F (5-HT
methodsMale mice were subjected to renal ischemia/reperfusion (I/R) and treated daily with lasmiditan (0.3 mg/kg) or vehicle beginning 24 h after injury for 3 or 6d. Serum creatinine was measured to estimate glomerular filtration. Electron microscopy was used to assess mitochondrial morphology and mitophagy. Mitochondrial-related protein were confirmed with immunoblotting. Mitochondrial function was assessed with ATP measurements.
resultsLasmiditan treatment improved mitochondrial and kidney recovery as early as 3d post-AKI, as evidenced by increased ATP, and decreased serum creatinine, respectively. Electron micrographs of renal cortices revealed that lasmiditan also decreased mitochondrial damage and increased mitochondrial area and size by 6d after I/R injury. Additionally, lasmiditan treatment increased mitolysosomes by 3d, indicating induction of mitophagy. Phosphorylation of mitophagy-related proteins were also increased in the renal cortices of lasmiditan-treated AKI mice 3d after I/R injury, whereas fusion-related proteins were increased at 6d after I/R injury.
conclusionThese data reveal that lasmiditan accelerates renal recovery, restores normal mitochondrial membrane and cristae morphology, decreases excessive mitochondrial fission, and accelerates mitophagy post-AKI in a time-dependent manner, establishing mitochondrial function and recovery from AKI.
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