| 研究実績の概要 |
Tensin2 (Tns2) deficiency results in alterations in podocytes and subsequent glomerular and tubulointerstitial injuries. However, this pathology is critically dependent on genetic background. While the Tns2-deficient podocytes of resistant murine strains, including C57BL/6J (B6) mice, remain almost intact, susceptible murine strains with Tns2 deficency, including ICGN mice, develop chronic kidney disease following alterations in the podocyte foot processes. Our data indicate that mouse chromosome 2 harbors two major genes associated with the severities of nephropathy. The proximal region on chromosome 2, Ttir, contributes to the resistance to tubulointerstitial fibrosis. In contrast, the distal region on chromosome 2, Tpir, contributes to the resistance to podocyte injury.
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