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The Protective Role of KANK1 in Podocyte Injury.
- Source :
-
International journal of molecular sciences [Int J Mol Sci] 2024 May 27; Vol. 25 (11). Date of Electronic Publication: 2024 May 27. - Publication Year :
- 2024
-
Abstract
- 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.
- Subjects :
- Animals
Humans
Male
Mice
Adaptor Proteins, Signal Transducing metabolism
Adaptor Proteins, Signal Transducing genetics
Apoptosis
Nephrotic Syndrome metabolism
Nephrotic Syndrome genetics
Nephrotic Syndrome pathology
Tumor Suppressor Proteins metabolism
Tumor Suppressor Proteins genetics
Cytoskeletal Proteins metabolism
Cytoskeletal Proteins genetics
Doxorubicin
Mice, Knockout
Podocytes metabolism
Podocytes pathology
Subjects
Details
- Language :
- English
- ISSN :
- 1422-0067
- Volume :
- 25
- Issue :
- 11
- Database :
- MEDLINE
- Journal :
- International journal of molecular sciences
- Publication Type :
- Academic Journal
- Accession number :
- 38891998
- Full Text :
- https://doi.org/10.3390/ijms25115808