The role of senescence marker protein-30 (SMP30) in the progression of diabetic nephropathy

衰老标记物蛋白-30(SMP30)随着年龄的增长而减少，并参与衰老的症状。本研究采用链脲佐菌素诱导的糖尿病SMP30基因敲除(KO)小鼠模型，探讨SMP30基因缺失在糖尿病肾病发病机制中的作用。在非糖尿病KO小鼠中观察到肾小管损伤伴肾小管间质纤维化，糖尿病加重了这些改变。另一方面，SMP30缺失并不影响肾小球的改变。HIF-1α积聚、氧化应激增加和肾小管炎症与肾小管损伤有关。结论：随着年龄的增长，SMP30的降低可能通过肾小管损害导致糖尿病肾病的进展。

Senescence marker protein-30 (SMP30) decreases with age and contributes to the symptoms of aging. In this study, we investigated the effect of SMP30 deficiency on the pathogenesis of diabetic nephropathy using streptozocin induced diabetic SMP30 knockout (KO) mice. Tubular damages with tubulointerstitial fibrosis were observed in non-diabetic KO mice, and diabetes exacerbated these changes. On the other hand, SMP30 deletion did not affect glomerular changes. The accumulation of HIF-1alpha, the increase of oxidative stress, and tubular inflammation were associated with tubular injuries. In conclusion, decreased SMP30 with age may contribute to the progression of diabetic nephropathy through tubular damages.