ArticleScientific reports2025
Targeting MCL1 by UMI-77 to induce mitophagy alleviates renal tubular epithelial cells injury in acute kidney injury.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Acute kidney injury (AKI) is a common clinical disease with complex pathophysiological processes and with high morbidity and mortality. Severe mitochondrial damages, such as mitochondrial swelling and fragmentation, disruption of membrane integrity, and broken or absent cristae, were observed in renal tubular epithelial cells (TECs) of ischemic AKI mice. However, whether artificial activation of mitophagy can alleviate TECs injury is still unknown. In this study, we tested the pro-mitophagy effect of UMI-77, which was identified as an unexpected mitophagy activator at sub-lethal doses in 2020, and verified the protective effect of activated mitophagy on TECs during AKI. We found that UMI-77 activates mitophagy in TECs and ameliorates kidney damage during AKI both in vivo and in vitro. This protective effect of UMI-77 on TECs can be reversed by adding mitophagy inhibitor Mdivi-1 or inhibiting the expression of mitophagy receptor MCL-1. These results indicate that UMI-77 mitigates TECs injury in AKI primarily through activating mitophagy, and artificial activation of mitophagy could be an effective strategy for treating AKI.
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