本文采用的英格恩产品: Entranter-R4000
The diagnostic value and mechanism of miR-127-3p in type 2 diabetes and complications of diabetic nephropathy
Affiliations
- 1 Department of Clinical Laboratory, Huangshi Central Hospital, Huangshi, 435000, Hubei, China.
- 2 Huangshi Key Laboratory of Molecular Diagnosis and Treatment of Tumors, Huangshi, 435000, China.
- 3 Nephrology Department, Shanghai Putuo District People’s Hospital, Shanghai, 200060, China.
- 4 Department of Endocrinology, Shenzhen Second People’s Hospital, Shenzhen, 518035, Guangdong, China.
- 5 Biology Faculty, Adam Mickiewicz University, Poznań, 61-712, Poland.
- 6 Department of Medical Laboratory Medicine, Chongqing University Fuling Hospital, No. 2 Gaosuntang Road, Fuling District, Chongqing, 408000, China. LuoguoxiaCQ@163.com.
- 7 Department of Rehabilitation Medicine, The Affiliated Hospital of Youjiang Medical University for Nationalities, No.18, Zhongshan 2nd Road, Youjiang District, Baise, Guangxi, 533000, China. cenmeini96@163.com.
- 8 Key Laboratory of Research and Development on Clinical Molecular Diagnosis for High-Incidence Diseases of Baise, No.18, Zhongshan 2nd Road, Youjiang District, Baise, Guangxi, China. cenmeini96@163.com.
- PMID: 41350748
- PMCID: PMC12798043
- DOI: 10.1186/s41065-025-00618-x
Abstract
Background: Diabetic kidney disease (DKD) is a serious microvascular complication of type 2 diabetes mellitus (T2DM). miR-127-3p is dysregulated in T2DM, but the specific molecular mechanism remains unclear. We aim to probe the diagnostic value of miR-127-3p and its molecular mechanism in T2DM and DKD.
Methods: This study comprised 218 individuals, including 78 patients with T2DM, 72 patients with DKD and 68 healthy controls. All participants underwent fasting peripheral blood collection. In vitro, we simulated a hyperglycemic environment by treating human mesangial cells (HMC) with high-concentration glucose (HG). Subsequently, RT-qPCR was used to detect the levels of miR-127-3p in serum and HMC. Cell viability and inflammatory cytokine (TNF-α, IL-1β and IL-6) levels were assessed using the CCK-8 assay and ELISA, respectively. The dual-luciferase reporter assay validated the target relationship between miR-127-3p and ACO2.
Results: By comparing baseline clinical characteristics, we identified significant differences among the three groups in high density lipoprotein cholesterol (HDL-C), triglycerides (TG), fasting blood glucose (FBG), glycated hemoglobin A1c (HbA1c), blood urea nitrogen (BUN), estimated glomerular filtration rate (eGFR) and albuminuria. Additionally, miR-127-3p was elevated in T2DM and DKD patients. It could distinguish healthy individuals from T2DM or T2DM from DKD. In HG-induced HMC, miR-127-3p inhibitor elevated the cell viability and the levels of SOD while suppressing the levels of MDA. These effects were abolished by ACO2 silencing. Furthermore, downregulated miR-127-3p reduced the levels of TNF-α, IL-1β and IL-6. sh-ACO2 alleviated the inhibitory effects of miR-127-3p.
Conclusions: Upregulated miR-127-3p was involved in the progression of T2DM and DKD. In HG-induced HMC, down-regulated miR-127-3p improved cell viability and suppressed oxidative stress and inflammatory responses by negatively regulating ACO2.
Keywords: ACO2; DKD; Inflammation; Oxidative stress; T2DM; miR-127-3p.
