Journal
LABORATORY INVESTIGATION
Volume 99, Issue 5, Pages 684-697Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41374-018-0176-7
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Funding
- National Natural Science Foundation of China [81870500, 81770714]
- Natural Science Foundation of Hunan Province [2017JJ2002]
- Health and Family Planning Commission of Hunan Province [20180922]
- Changde Municipal Science and Technology Bureau
- [2016KZ34]
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Diabetic kidney disease (DKD) is the leading cause of morbidity and mortality in individuals with diabetes, and it is the leading cause of end-stage renal disease (ESRD) worldwide. Stanniocalcin-1 (STC-1) is present in various tissues, and it has antioxidant and anti-apoptotic activities, which play a role in kidney protection, including diabetic nephropathy (DN). However, the mechanism that underlies these effects remains unknown. This study suggests that STC-1 ameliorates oxidative stress and cell apoptosis in the kidneys of db/db mice and high glucose (HG)-treated BUMPT cells by inhibiting Bnip3 expression through AMPK/Sirt3 pathway activation. In the clinic, DKD patients with high levels of STC-1 have a better prognosis than patients with low STC-1 levels. Thus, we concluded that STC-1 ameliorates renal injury in DN by inhibiting the expression of Bnip3 through the AMPK/SIRT3 pathway and that serum STC-1 is independently associated with DKD progression in patients with type 2 diabetes. As high STC-1 levels indicate a better prognosis, synthetic STC-1 may become a potential drug for the treatment of DKD patients.
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