ArticleMolecular therapy. Nucleic acids2020
Upregulation of miR-101a Suppresses Chronic Renal Fibrosis by Regulating KDM3A via Blockade of the YAP-TGF-β-Smad Signaling Pathway.
Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 45 citations in OpenAlex.
- Selective blockade of latent TGF-β1 activation suppresses tissue fibrosis with good safety.Communications medicine · 2026Article
- Multidimensional Regulatory Network ofOncology research · 2026Review
- METTL3-driven mFrontiers in immunology · 2026Article
- Key RNA-binding proteins in renal fibrosis: a comprehensive bioinformatics and machine learning framework for diagnostic and therapeutic insights.Renal failure · 2025Article
- The novel regulatory role of miR-101a in CRH expression following low-concentration DEHP exposure in zebrafish embryos.Functional & integrative genomics · 2025Article
- Exploring the Role of miRNA-101a in the Circulatory System's Adaptive Mechanisms in Hypertensive Disorders of Pregnancy.Diagnostics (Basel, Switzerland) · 2025Article
- Mechanism of TGIF1 on glycolipid metabolism disorders in mice with type 2 diabetes.BMJ open diabetes research & care · 2025Article
- MiR-92a-3p Promotes Renal Injury and Fibrosis Through Facilitating M1 Macrophage Polarization via Targeting LIN28A.Physiological research · 2024Article
- Reviewing the Regulators of COL1A1.International journal of molecular sciences · 2023Review
- Identification of transcription factors related to diabetic tubulointerstitial injury.Journal of translational medicine · 2023Article
- Epigenetics as a versatile regulator of fibrosis.Journal of translational medicine · 2023Review
- Up-regulation of the human-specific CHRFAM7A gene protects against renal fibrosis in mice with obstructive nephropathy.Journal of cellular and molecular medicine · 2023Article
- Association between Circulating MicroRNAs (miR-21-5p, miR-20a-5p, miR-29b-3p, miR-126-3p and miR-101-3p) and Chronic Allograft Dysfunction in Renal Transplant Recipients.International journal of molecular sciences · 2022Article
- The Hippo pathway and its correlation with acute kidney injury.Zoological research · 2022Review
- WTAP-mediated NCellular & molecular biology letters · 2022Article
- Lysine demethylase 3A is a positive regulator of cardiac myofibroblast transdifferentiation that increases Smad3 phosphorylation following transforming growth factor beta1 stimulation.Molecular biology reports · 2022Article
- Depleted HDAC3 attenuates hyperuricemia-induced renal interstitial fibrosis via miR-19b-3p/SF3B3 axis.Cell cycle (Georgetown, Tex.) · 2022Article
- microRNA-20-1 and microRNA-101a Suppress the NF-κB-Mediated Inflammation Production by Targeting TRAF6 in Miiuy Croaker.Infection and immunity · 2022Article
- The role of YAP1 in survival prediction, immune modulation, and drug response: A pan-cancer perspective.Frontiers in immunology · 2022Article
- Mechanism of miR-365 in regulating BDNF-TrkB signal axis of HFD/STZ induced diabetic nephropathy fibrosis and renal function.International urology and nephrology · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal fibrosis denotes a common complication of diabetic nephropathy and is a predominant cause of end-stage renal disease. Despite the association between microRNAs (miRNAs or miRs) and renal fibrosis, miRNAs have been reported to play a vital role in the development of chronic renal fibrosis. Therefore, the aim of the present study was to investigate the possible function of miR-101a in chronic renal fibrosis. Initially, microarray-based gene expression profiling of renal fibrosis was employed to screen the differentially expressed genes. An in vivo mouse model of chronic renal fibrosis induced by a unilateral ureteral obstruction (UUO) and an in vitro cell model induced by aristolochic acid (AA) were constructed. miR-101a expression was examined using a fluorescence in situ hybridization (FISH) assay and quantitative reverse transcription polymerase chain reaction (qRT-PCR). Then, the interaction between miR-101a and KDM3A was identified using an online website combined with a dual-luciferase reporter assay. Finally, gain- and loss-of-function experiments were conducted to elucidate the effect of miR-101a on the expression of Col1a1, fibronectin, α-smooth muscle actin (α-SMA), and YAP-TGF-β (transforming growth factor β)-Smad signaling pathway-related genes, as well as the degree of renal fibrosis. miR-101a was poorly expressed while KDM3A was robustly induced in chronic renal fibrosis tissues and cells. In addition, miR-101a could target and downregulate KDM3A expression, which led to elevated TGIF1, inhibited expression of Collagen I (Col1a1), fibronectin, α-SMA, YAP1, and TGF-β2 along with the extent of Smad2/3 phosphorylation, as well as delayed renal fibrosis degree. Besides, overexpressed YAP/TGF-β2 or inhibited TGIF1 partially restored the inhibitory effect of miR-101a on chronic renal fibrosis. Taken together, miR-101a could potentially slow down chronic renal fibrosis by the inactivation of the YAP-TGF-β-Smad signaling pathway via KDM3A, highlighting the potential of miR-101a as a therapeutic target for chronic renal fibrosis treatment.
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