ArticleCellular and molecular life sciences : CMLS2023
FKBP5 deficiency attenuates calcium oxalate kidney stone formation by suppressing cell-crystal adhesion, apoptosis and macrophage M1 polarization via inhibition of NF-κB signaling.
Article in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 37 citations in OpenAlex.
- β-carotene attenuates calcium oxalate crystal-induced renal injury through suppression of NF-κB-mediated inflammation.Urolithiasis · 2026Article
- Targeting GLS and LPIN2 in renal fibroblasts: potential therapeutic targets for kidney stone disease identified by integrated multi-omics analysis.Urolithiasis · 2026Article
- Animal models for calcium oxalate kidney stone research.Zoological research · 2026Review
- IL-6 exacerbates calcium oxalate kidney stones by promoting inflammatory responses and crystal adhesion via p38 MAPK signaling activation.Urolithiasis · 2026Article
- GAS5 mediates notch signaling to exacerbate calcium oxalate-induced renal injury through the NF-κB/NLRP3 axis by promoting macrophage polarization.Cellular and molecular life sciences : CMLS · 2026Article
- ACAA1 mediates arachidonic acid dysregulation and membrane phospholipid remodeling to promote crystal-cell adhesion and ferroptosis susceptibility in calcium oxalate kidney stone.Journal of pharmaceutical analysis · 2026Article
- Paeoniflorin alleviates nephrolithiasis by targeting serpine1 and inhibiting the NF-κB signaling pathway.Urolithiasis · 2026Article
- Salidroside attenuates calcium oxalate-induced renal injury via suppression of PANoptosis.Urolithiasis · 2026Article
- Kidney adverse events associated with calcineurin inhibitors: a real-world study based on the FAERS database and network pharmacology.Frontiers in medicine · 2026Article
- M2 Macrophages Attenuate AQP2Research (Washington, D.C.) · 2026Article
- Ginsenoside Ro alleviated cuproptosis induced by high oxalate via inhibiting zinc transporter ZnT1 in renal tubular epithelial cells.Journal of ginseng research · 2026Article
- The mechanism and clinical significance of FKBP5 gene DNA methylation in various psychiatric, metabolic and tumor-related diseases.Frontiers in genetics · 2026Review
- Interleukin-38 Ameliorates Atherosclerosis by Inhibiting Macrophage M1-like Polarization and Apoptosis.Biomolecules · 2025Article
- AR Deficiency Protects Against Sepsis-Induced Acute Lung Injury by Inhibiting Macrophage M1 Polarization and Inflammatory Cytokine Secretion.Inflammation · 2025Article
- Linoelaidic acid alleviates COM-induced kidney injury and crystal deposition via the PPARγ/MAPK signaling pathway.Urolithiasis · 2025Article
- Macrophage Reprogramming: Emerging Molecular Therapeutic Strategies for Nephrolithiasis.Biomolecules · 2025Review
- Prediction of calcium oxalate kidney stones: A comprehensive analysis of clinical and gut microbiome characteristics.Medicine · 2025Article
- Inhibition of LINC00707/miR-223-3p/FKBP5 axis has a protective effect on diabetic kidney disease.Journal of diabetes investigation · 2025Article
- Molecular insights into cell signaling pathways in kidney stone formation.Urolithiasis · 2025Review
- Review
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Authors and funding
8 authors at 1 institution in 1 country.
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Abstract
Surgical crushing of stones alone has not addressed the increasing prevalence of kidney stones. A promising strategy is to tackle the kidney damage and crystal aggregation inherent in kidney stones with the appropriate therapeutic target. FKBP prolyl isomerase 5 (FKBP5) is a potential predictor of kidney injury, but its status in calcium oxalate (CaOx) kidney stones is not clear. This study attempted to elucidate the role and mechanism of FKBP5 in CaOx kidney stones. Lentivirus and adeno-associated virus were used to control FKBP5 expression in a CaOx kidney stone model. Transcriptomic sequencing and immunological assays were used to analyze the mechanism of FKBP5 deficiency in CaOx kidney stones. The results showed that FKBP5 deficiency reduced renal tubular epithelial cells (RTEC) apoptosis and promoted cell proliferation by downregulating BOK expression. It also attenuated cell-crystal adhesion by downregulating the expression of CDH4. In addition, it inhibited M1 polarization and chemotaxis of macrophages by suppressing CXCL10 expression in RTEC. Moreover, the above therapeutic effects were exerted by inhibiting the activation of NF-κB signaling. Finally, in vivo experiments showed that FKBP5 deficiency attenuated stone aggregation and kidney injury in mice. In conclusion, this study reveals that FKBP5 deficiency attenuates cell-crystal adhesion, reduces apoptosis, promotes cell proliferation, and inhibits macrophage M1 polarization and chemotaxis by inhibiting NF-κB signaling. This provides a potential therapeutic target for CaOx kidney stones.
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