Klotho inhibits renal oxidized low-density lipoprotein (ox-LDL) deposition via IGF-1R/RAC1/OLR1 signaling to ameliorate podocyte injury in diabetic kidney disease
Authors' conclusion
Our findings suggested that Klotho had the potential to mitigate podocyte injury and reduced high glucose-induced ox-LDL deposition in glomerulus by modulating the IGF-1R/RAC1/OLR1 signaling. These results provided valuable insights that could inform the development of novel strategies for diagnosing and treating DKD.
Study context
- Population
- Patients diagnosed with diabetic kidney disease (DKD) (serum and kidney biopsy samples); Streptozotocin (STZ)-induced DKD mice with Klotho genotype; podocytes in vitro
- Outcome
- Klotho and renal ox-LDL deposition
Methodological detailshuman serum and kidney biopsy samples, STZ-induced mouse model of DKD with Klotho genotype, in vitro podocyte experiments
- Human serum and kidney biopsy samples
- STZ-induced mouse model of DKD with Klotho genotype
- In vitro podocyte experiments
Main finding
As reported in the abstract
- Soluble Klotho inhibited high glucose-induced ox-LDL deposition in DKD podocytes
- Klotho reduced IGF-1R expression, decreasing RAC1 expression and enhancing mitochondrial function
- Significant reduction in OLR1 expression, with decreased renal ox-LDL deposition in DKD
Original publication
Klotho inhibits renal ox-LDL deposition via IGF-1R/RAC1/OLR1 signaling to ameliorate podocyte injury in diabetic kidney disease. Cardiovasc Diabetol. Published 27 October 2023. doi:10.
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