ArticleKidney & blood pressure research2025
ACOT4 and ACOT6 Activate Akt-mTOR Pathway and Inhibit Calcium Oxalate-Induced Renal Tubular Cell Injury.
Article in Kidney & blood pressure research, 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.
- Maternal protein restriction programs the ageing kidney: Proteomic signatures of early-life origin renal and metabolic dysfunction.The Journal of physiology · 2026Article
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7 authors.
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Abstract
introductionKidney stone caused by calcium oxalate (CaOx) is a chronic kidney disease. Acyl-coenzyme A thioesterases (ACOTs) serve as the key regulators of fatty acid metabolism. However, ACOTs' effect on CaOx kidney stone formation remains to be explored. Here, we aimed to investigate the effect of ACOTs on CaOx kidney stone formation.
methodsHK-2 and M-1 cells were cultured in DMEM/F12 medium supplemented with 10% FBS. Cells were treated with varying concentrations of calcium oxalate (CaOx) and transfected with siRNA or plasmid vectors targeting ACOT4 and ACOT6 using Lipofectamine RNAiMAX or Lipofectamine 3000. RT-qPCR and Western blotting were used to analyze gene and protein expression. Cell viability was assessed with CCK-8, and cell apoptosis was measured by flow cytometry. Crystal adhesion was visualized under a microscope. Lactate dehydrogenase (LDH) release was measured using a cytotoxicity assay kit. A kidney stone mouse model was established by injecting glyoxylic acid to induce kidney stones, and tissues were analyzed by Western blotting.
resultsThe mRNA and protein levels of several ACOT family members were upregulated in HK-2 cells treated with CaOx (inducing cell injury). Knockdown of ACOT4 and ACOT6 significantly suppressed the activity of CaOx-pretreated HK-2 and M-1 cells, and promoted the crystal formation and LDH release, whereas overexpression of ACOT4 and ACOT6 reduced CaOx crystal-induced kidney cell injury. Furthermore, the levels of p-AKT and p-S6 decreased after ACOT4 and ACOT6 knockdown and increased following ACOT4 and ACOT6 overexpression, suggesting that both ACOT4 and ACOT6 activated Akt/mTOR signaling pathway in HK-2 cells. We also observed that knockdown of ACOT4 and ACOT6 induced the apoptosis of HK-2 cells after CaOx treatment. Inhibition of apoptosis using Z-VAD-FMK reversed the enhanced cell injury caused by CaOx treatment and ACOT4/6 knockdown, suggesting that knockdown of ACOT4 and ACOT6 promoted cell injury via inducing cell apoptosis.
conclusionsACOT4 and ACOT6 could be protecting factors for kidney cell injury induced by CaOx via reducing apoptosis and activating Akt/mTOR signaling pathway. The study of the role of ACOT4 and ACOT6 in kidney cell injury provides a new insight into the cause of CaOx kidney stone formation. Its in-depth study may provide new targets for stone treatment.
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