| First Author | Oda K | Year | 2024 |
| Journal | Int J Mol Sci | Volume | 25 |
| Issue | 11 | PubMed ID | 38891998 |
| Mgi Jnum | J:354142 | Mgi Id | MGI:7659708 |
| Doi | 10.3390/ijms25115808 | Citation | Oda K, et al. (2024) The Protective Role of KANK1 in Podocyte Injury. Int J Mol Sci 25(11) |
| abstractText | Approximately 30% of steroid-resistant nephrotic syndromes are attributed to monogenic disorders that involve 27 genes. Mutations in KANK family members have also been linked to nephrotic syndrome; however, the precise mechanism remains elusive. To investigate this, podocyte-specific Kank1 knockout mice were generated to examine phenotypic changes. In the initial assessment under normal conditions, Kank1 knockout mice showed no significant differences in the urinary albumin-creatinine ratio, blood urea nitrogen, serum creatinine levels, or histological features compared to controls. However, following kidney injury with adriamycin, podocyte-specific Kank1 knockout mice exhibited a significantly higher albumin-creatinine ratio and a significantly greater sclerotic index than control mice. Electron microscopy revealed more extensive foot process effacement in the knockout mice than in control mice. In addition, KANK1-deficient human podocytes showed increased detachment and apoptosis following adriamycin exposure. These findings suggest that KANK1 may play a protective role in mitigating podocyte damage under pathological conditions. |
