ArticleFrontiers in pharmacology2018
miR-374a Regulates Inflammatory Response in Diabetic Nephropathy by Targeting MCP-1 Expression.
Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- The Immunological Microenvironment and the Emerging Role of Stem Cells Therapy in Peyronie's Disease: A Systematic Narrative Review.International journal of molecular sciences · 2023Pooled it
- Determination of microRNAs associated with adverse left ventricular remodeling after myocardial infarction.Molecular and cellular biochemistry · 2022Trial
- MiR-509-3p Targets YAP1 to Regulate Inflammatory Cytokines Against Hyperglycemia-Induced Renal Tubular Cell Damage in Diabetic Kidney Disease.Combinatorial chemistry & high throughput screening · 2026Article
- Dysregulation of miR-21-5p in diabetic nephropathy and its role in inflammatory response.Journal of diabetes investigation · 2025Article
- mTOR pathway: A key player in diabetic nephropathy progression and therapeutic targets.Genes & diseases · 2025Review
- Plasma MCP-1 and TGF-β1 Levels are Associated with Kidney Injury in Children with Congenital Anomalies of the Kidney and Urinary Tract.Applied biochemistry and biotechnology · 2024Article
- The role of innate immunity in diabetic nephropathy and their therapeutic consequences.Journal of pharmaceutical analysis · 2024Review
- Circular RNA COL1A2 Mediates High Glucose-Induced Oxidative Stress and Pyroptosis by Regulating MiR-424-5p/SGK1 in Diabetic Nephropathy.Applied biochemistry and biotechnology · 2023Article
- Article
- Relationship between Macrophages and Tissue Microenvironments in Diabetic Kidneys.Biomedicines · 2023Review
- Autologous blood transfusion impedes glycolysis in macrophages to inhibit red blood cell injury in type 2 diabetes through PI3K/Akt/PKM2 signaling axis.Acta diabetologica · 2023Article
- Crosstalk between proximal tubular epithelial cells and other interstitial cells in tubulointerstitial fibrosis after renal injury.Frontiers in endocrinology · 2023Review
- Sex-biased expression of selected chromosome x-linked microRNAs with potent regulatory effect on the inflammatory response in children with cystic fibrosis: A preliminary pilot investigation.Frontiers in immunology · 2023Article
- miR-374a-5p regulates inflammatory genes and monocyte function in patients with inflammatory bowel disease.The Journal of experimental medicine · 2022Article
- Loss of RNA binding protein HuD facilitates the production of the senescence-associated secretory phenotype.Cell death & disease · 2022Article
- SETD8 cooperates with MZF1 to participate in hyperglycemia-induced endothelial inflammation via elevation of WNT5A levels in diabetic nephropathy.Cellular & molecular biology letters · 2022Article
- Epac activation ameliorates tubulointerstitial inflammation in diabetic nephropathy.Acta pharmacologica Sinica · 2022Article
- Epigenetics in the pathogenesis of diabetic nephropathy.Acta biochimica et biophysica Sinica · 2022Review
- Immune responses in diabetic nephropathy: Pathogenic mechanisms and therapeutic target.Frontiers in immunology · 2022Review
- Rack1 regulates pro-inflammatory cytokines by NF-κB in diabetic nephropathy.Open medicine (Warsaw, Poland) · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The microRNA (mir)-374a has been implicated in several types of human cancer; however, its role in diabetic nephropathy (DN) remains unclear. Monocyte chemoattractant protein (MCP)-1 is a chemokine that recruits macrophages to inflammatory sites and is important for the development and progression of DN. However, the relationship between miR-374a and MCP-1 in DN is unknown. We addressed this in the present study by examining the expression of these factors in kidney tissue samples from DN patients and through loss- and gain-of-function experiments using HK2 human renal tubular epithelial cells. We found that miR-374a was downregulated whereas MCP-1 was upregulated in DN tissue. A bioinformatics analysis revealed that MCP-1 is a putative target of miR-374a. To confirm this relationship, HK2 cells treated with normal glucose (5.6 mmol/l D-glucose), high glucose (HG) (30 mmol/l D-glucose), or high osmotic pressure solution (5.6 mmol/l D-glucose + 24.4 mmol/l D-mannitol) were transfected with miR-374a mimic or inhibitor. miR-374a mimic reduced MCP-1 mRNA expression and migration of co-cultured U937 cells, whereas miR-374a inhibition had the opposite effects. Additionally, interleukin-6 and -18 and tumor necrosis factor-α levels were downregulated by transfection of miR-374a mimic. On the other hand, MCP-1 overexpression reversed the inhibitory effects of miR-374a in HK2 cells. Thus, miR-374a suppresses the inflammatory response in DN through negative regulation of MCP-1 expression. These findings suggest that therapeutic strategies that target the miR-374a/MCP-1 axis can be an effective treatment for DN.
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