ArticleBMC nephrology2019
Intrarenal microRNA signature related to the fibrosis process in chronic kidney disease: identification and functional validation of key miRNAs.
Article in BMC nephrology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 37 citations in OpenAlex.
- Modulation of miR-29a and miR-29b Expression and Their Target Genes Related to Inflammation and Renal Fibrosis by an Oral Nutritional Supplement with Probiotics in Malnourished Hemodialysis Patients.International journal of molecular sciences · 2024Trial
- Integrative Analyses of Circulating Small RNAs and Kidney Graft Transcriptome in Transplant Glomerulopathy.International journal of molecular sciences · 2021Trial
- Obesity-Related Chronic Kidney Disease: From Diagnosis to Treatment.Diagnostics (Basel, Switzerland) · 2025Review
- A Systematic Review and Meta-Analysis of microRNA Profiling Studies in Chronic Kidney Diseases.Non-coding RNA · 2024Review
- LncRNA SNHG1 knockdown inhibits hyperglycemia induced ferroptosis via miR-16-5p/ACSL4 axis to alleviate diabetic nephropathy.Journal of diabetes investigation · 2023Article
- The Role of miRNA in Renal Fibrosis Leading to Chronic Kidney Disease.Biomedicines · 2023Review
- Epigenetic Mechanisms and Nephrotic Syndrome: A Systematic Review.Biomedicines · 2023Review
- Ochratoxin A induces endoplasmic reticulum stress and fibrosis in the kidney via the HIF-1α/miR-155-5p link.Toxicology reports · 2023Article
- Therapeutic potential of urine exosomes derived from rats with diabetic kidney disease.Frontiers in endocrinology · 2023Article
- miRNA biomarkers in renal disease.International urology and nephrology · 2022Review
- MicroRNA miR-4709-3p targets Large Tumor Suppressor Kinase 2 (LATS2) and induces obstructive renal fibrosis through Hippo signaling.Bioengineered · 2021Article
- MiR-142-3p ameliorates high glucose-induced renal tubular epithelial cell injury by targeting BOD1.Clinical and experimental nephrology · 2021Article
- MicroRNA-10 negatively regulates inflammation in diabetic kidney via targeting activation of the NLRP3 inflammasome.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Article
- Fibrosis in Chronic Kidney Disease: Pathogenesis and Consequences.International journal of molecular sciences · 2021Review
- Article
- Deciphering the Pharmacological Mechanisms of Taohe-Chengqi Decoction Extract Against Renal Fibrosis Through Integrating Network Pharmacology and Experimental ValidationFrontiers in pharmacology · 2020Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThough the roles of microRNAs (miRNAs) in renal diseases have been extensively investigated, a thorough screening and comparison of miRNAs among different types of chronic kidney disease (CKD) has never been performed.
methodsThe intrarenal miRNAs were profiled from fresh kidney tissues of patients with biopsy-proven minimal change disease (MCD), focal segmental glomerular sclerosis (FSGS) and diabetic nephropathy (DN) by using microarray. Commonly dysregulated miRNAs were validated by real-time PCR using paraffin-embedded renal tissues from all three types of CKD patients as well as mouse unilateral ureteral obstruction (UUO) model. Two novel miRNAs were selected and annotations of their target genes were performed using GO and KEGG pathway enrichment analysis. Biological functions of three two candidate miRNAs were explored in TGF-β1-induced cell model using human kidney proximal tubular cells (HK-2).
resultsThe kidney biopsy samples of three disease types represent different levels of damage and fibrosis, which were the mildest in MCD, moderate in FSGS, and the most severe in DN. 116 miRNAs were identified to be commonly dysregulated, including 40 up-regulated and 76 down-regulated in CKD tissues as compared with healthy donor kidney biopsy tissues. Two novel miRNAs, hsa-miR-3607-3p and hsa-miR-4709-3p, were verified as consistently differentially expressed among all three types of patient samples as well as in mouse model. In vitro, hsa-miR-3607-3p was repressed while hsa-miR-4709-3p was induced by TGF-β1 treatment. Inhibition of hsa-miR-3607-3p or overexpression of hsa-miR-4709-3p promoted TGF-β1-induced migration and F-actin assembling in HK-2 cells, which are characteristics of epithelial-mesenchymal transition (EMT). Further study identified that ITGB8 and CALM3 were the bona fide target genes of hsa-miR-3607-3p and hsa-miR-4709-3p respectively.
conclusionsThe present identify a unique miRNAs profile that probably relates to the common fibrosis process of CKD. Results of our study suggest that hsa-miR-3607-3p and hsa-miR-4709-3p may represent as promising therapeutic targets against kidney fibrosis.
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