ArticleJournal of translational medicine2024
ABI3BP promotes renal aging through Klotho-mediated ferroptosis.
Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Characterization of Umbilical Cord Mesenchymal Stromal Cells Overexpressing Klotho and In Vitro Anti-Aging Efficacy of Their Derived Extracellular Vesicles.International journal of molecular sciences · 2026Article
- Abnormal lipid metabolism in senescent renal tubular cells in diabetic nephropathy.Cellular and molecular life sciences : CMLS · 2026Review
- Klotho protects the osteogenic function of human periodontal ligament stem cells in periodontitis by inhibiting NOX4-mediated ferroptosis.Stem cell research & therapy · 2026Article
- Targeting Ferroptosis to Eliminate Senescent Cells: Mechanisms and Therapeutic Potential.Aging and disease · 2025Review
- Renoprotective effects of GHRH agonist MR409 is associated with reduced oxidative stress and ferroptosis in diabetic mice.Frontiers in pharmacology · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
The aging process of the kidneys is accompanied with several structural diseases. Abnormal fiber formation disrupts the balance of kidney structure and function, causing to end-stage renal disease and subsequent renal failure. Despite this, the precise mechanism underlying renal damage in aging remains elusive. In this study, ABI3BP gene knockout mice were used to investigate the role of ABI3BP in renal aging induced by irradiation. The results revealed a significant increase in ABI3BP expression in HK2 cells and kidney tissue of aging mice, with ABI3BP gene knockout demonstrating a mitigating effect on radiation-induced cell aging. Furthermore, the study observed a marked decrease in Klotho levels and an increase in ferroptosis in renal tissue and HK2 cells following irradiation. Notably, ABI3BP gene knockout not only elevated Klotho expression but also reduced ferroptosis levels. A significant negative correlation between ABI3BP and Klotho was established. Further experiments demonstrated that Klotho knockdown alleviated the aging inhibition caused by ABI3BP downregulation. This study identifies the upregulation of ABI3BP in aged renal tubular epithelial cells, indicating a role in promoting ferroptosis and inducing renal aging by inhibiting Klotho expression.
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