ArticleClinical science (London, England : 1979)2025
SUL-138 mitigates accelerated endothelial aging and protects the kidney.
Article in Clinical science (London, England : 1979), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Tagln1-Cre-driven Ercc1 deficiency reveals sex-specific effects on adipose tissue in mice.Endocrinology · 2026Article
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18 authors.
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Abstract
Vascular aging is marked by increased levels of reactive oxygen species in endothelial cells. Reactive oxygen species can, among others, be produced by dysfunctional mitochondria, contributing to acceleration of vascular aging by promoting DNA damage response and senescence. In the aged vasculature, impaired endothelial cell function causes decreased vasodilation, which may also have an impact on peripheral organs such as the kidney. The aim of this study was to investigate the effect of chronic treatment with SUL-138 (30 mg/kg/day), a novel mitochondrial protective compound, on DNA damage-prompted, accelerated endothelial aging and associated kidney dysfunction in mice. Endothelial-specific aging was induced by knock-out (KO) of DNA repair endonuclease Ercc1 in mice [endothelial-cell specific Ercc1 KO (EC-KO) mice]. We showed that impaired endothelium-dependent vasodilation and expression of DNA damage response markers in EC-KO mice were restored after the treatment with SUL-138. The underlying mechanism of improved vasodilation was an increase in endothelium-derived hyperpolarization (EDH). Endothelial-specific aging induced tubular injury, sodium wasting, and increased inflammatory markers in the kidney, which were normalized by the treatment with SUL-138. We conclude that accelerated endothelial aging adversely affects vascular function and causes kidney tubular injury. SUL-138 rescues endothelial aging, restores vasodilation by increasing EDH, and protects the kidney. Thus, preservation of mitochondrial function is a potential pharmacotherapeutic target in aging-related dysfunction provoked by the DNA damage response.
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