ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2020
LncRNA SNHG16 Aggravates High Glucose-Induced Podocytes Injury in Diabetic Nephropathy Through Targeting miR-106a and Thereby Up-Regulating KLF9.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 29 citations in OpenAlex.
- A Global Transcriptomic Analysis Reveals Body Weight-Specific Molecular Responses to Chronic Orange Juice Consumption in Healthy Individuals.Molecular nutrition & food research · 2025Article
- Sunitinib-resistant renal cell carcinoma cell-derived exosomes promote facilitation of tumor progression via secretion of the lncRNA SNHG16.Human cell · 2025Article
- The Role of Antioxidant Transcription Factor Nrf2 and Its Activating Compounds in Systemic Lupus Erythematosus.Antioxidants (Basel, Switzerland) · 2024Review
- STAT3-induced upregulation of lncRNA TTN-AS1 aggravates podocyte injury in diabetic nephropathy by promoting oxidative stress.Toxicology research · 2024Article
- Downregulating lncRNA MIAT attenuates apoptosis of podocytes exposed to high glucose.Acta diabetologica · 2024Article
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- Silencing LncRNA SNHG16 suppresses the diabetic inflammatory response by targeting the miR-212-3p/NF-κB signaling pathway.Diabetology & metabolic syndrome · 2023Article
- LncRNA SNHG16 regulates RAS and NF-κB pathway-mediated NLRP3 inflammasome activation to aggravate diabetes nephropathy through stabilizing TLR4.Acta diabetologica · 2023Article
- Oxidative stress and inflammation in diabetic nephropathy: role of polyphenols.Frontiers in immunology · 2023Review
- Enhanced Orai1-mediated store-operated CaThe Journal of biological chemistry · 2022Article
- MiR-106a facilitates the sensorineural hearing loss induced by oxidative stress by targeting connexin-43.Bioengineered · 2022Article
- Regulation of Oxidative Stress by Long Non-Coding RNAs in Vascular Complications of Diabetes.Life (Basel, Switzerland) · 2022Review
- Long Non-Coding RNAs in the Pathogenesis of Diabetic Kidney Disease.Frontiers in cell and developmental biology · 2022Review
- Interference of KLF9 relieved the development of gestational diabetes mellitus by upregulating DDAH2.Bioengineered · 2022Article
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Authors and funding
2 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
introductionDiabetic nephropathy (DN) is one of the major complications of diabetes and podocyte injury plays an important role in the DN pathogenesis. MicroRNA (miR)-106a is predicated to be a target of long noncoding RNA (lncRNA) SNHG16 and has been identified as a therapeutic biomarker for diabetic kidney diseases. However, the role of SNHG16/miR-106a axis in DN has not been illustrated. This study aimed to investigate whether SNHG16 could regulate podocyte injury via miR-106a in DN and uncover the underlying mechanism.
methodsMPC5 podocytes were treated with control or high glucose (HG) medium, and then miR-106a level was measured. MPC5 cells that exposed to HG were overexpressed with miR-106a or not, following by overexpression with or without KLF9 or SNHG16. Then, cell viability, apoptosis, reactive oxygen species and the protein expression of synaptopodin and podocin were evaluated.
resultsMiR-106a was down-regulated in the serum of DN patients and HG-induced MPC5 podocytes. Overexpression of miR-106a suppressed HG-induced decrease in cell viability, Bcl-2, synaptopodin and podocin expression, increase in ROS, apoptotic cells, Bax and cleaved-caspase 3 expression. MiR-106a could bind to both KLF9 and lncRNA SNHG16, which were up-regulated in the serum of DN patients and HG-induced MPC5 podocytes. The level of miR-106a was decreased by SNHG16 overexpression and miR-106a overexpression reduced KLF9 expression. Furthermore, overexpression of KLF9 or SNHG16 blunted the protective effects of miR-106a on HG-induced MPC5 injury. DISCUSSION: LncRNA SNHG16 could promote HG-stimulated podocytes injury via targeting miR-106a to enhance KLF9 expression. The intervention of SNHG16/miR-106a/KLF9 may be a therapeutic treatment for DN.
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