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Last update 08 May 2025

MIR139

Last update 08 May 2025

Basic Info

Synonyms

hsa-mir-139, microRNA 139, MIR139

+ [1]

Introduction-

Drugs associated with MIR139

US20240150765

Patent Mining

Target

MIR129 x MIR139 x MIR140 x MIR194 x miR-145 x miR-15a x miR-16 x miR-192

Mechanism-

Active Org.

Curamir Therapeutics, Inc.

Originator Org.

Curamir Therapeutics, Inc.

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MIR139

100 Translational Medicine associated with MIR139

0 Patents (Medical) associated with MIR139

665

Literatures (Medical) associated with MIR139

01 Apr 2025·Endocrine Connections

Inhibition of microRNA-139-5p by glucagon-like peptide-1 ameliorates oxidative stress-induced damage via targeting SOD1/GCLc

Article

Author: Mo, Zhaohui ; Xiong, Jing ; Fu, Lanfang ; Meng, Xubiao ; Zhang, Jiaqi ; Mo, Jiake ; Liu, Ying ; Tang, Weian

Oxidative stress is a key driving factor for the progression of vascular disease in diabetes, and is closely related to endothelial dysfunction. The exact mechanism by which glucagon-like peptide-1 (GLP-1) directly protects vascular endothelium by reducing oxidative stress is not yet fully understood. In this study, we investigated the protective effect of GLP-1 on endothelial cells exposed to palmitate/high glucose-induced oxidative stress and further explored the potential mechanisms involved in microRNA-139-5p (miR-139-5p) regulation. We found that miR-139-5p expression was exhibited significantly elevated in HUVECs that were exposed to palmitate/high glucose or H2O2, which were reversed by glutathione. Interestingly, this expression was significantly attenuated after GLP-1 pretreatment, with reduced ROS, increased GSH/GSSG ratio and amelioration of cell dysfunction. Overexpression of miR-139-5p resulted in increased ROS and apoptosis, decreased GSH/GSSG ratio, damaged migration and proliferation of HUVECs, while inhibition of miR-139-5p significantly restored palmitate-induced HUVECs impairments. Further investigation revealed that miR-139-5p directly targets superoxide dismutase 1(SOD1)/ glutamate-cysteine ligase catalytic subunit(GCLc). The upregulation of miR-139-5p abrogated the protective effects of GLP-1 on cells exposed to palmitate, and GLP-1-induced downregulation of miR-139-5p was counteracted by the GLP-1 receptor antagonist Exendin(9-39). These findings demonstrated that GLP-1 ameliorates oxidative stress-induced endothelial dysfunction, at least in part, by suppressing miR-139-5p, which targets SOD1 and GCLc. This provides further evidence for the vascular protective effects of GLP-1 intervention in diabetes.

20 Jan 2025·Nan fang yi ke da xue xue bao = Journal of Southern Medical University

Differential expressions of exosomal miRNAs in patients with chronic heart failure and hyperuricemia: diagnostic values of miR-27a-5p and miR-139-3p.

Article

Author: Huang, Xia ; Chen, Zhiliang ; Qu, Yuan ; Yang, Yonggang ; Gu, Ning ; Heng, Qiqi ; Fu, Yujia ; Cheng, Yan ; Li, Kewei

OBJECTIVESTo analyze the differentially expressed exosomal miRNAs in patients with chronic heart failure (CHF) complicated by hyperuricemia (HUA) and explore their potential as novel diagnostic molecular markers and their target genes.METHODSThis study was conducted among 30 CHF patients with HUA (observation group) and 30 healthy volunteers (control group) enrolled between September, 2020 and September, 2023. Peripheral blood samples were collected from 6 CHF patients with HUA for analyzing exosomal miRNAs by high-throughput sequencing, and the results were validated in the remaining 24 patients using qRT-PCR. GO and KEGG enrichment analyses were performed to predict the the target genes of the identified differential miRNAs. We also validated the differentially expressed miRNAs by animal experiment.RESULTSA total of 42 differentially expressed exosomal miRNAs were detected in observation group by high-throughput sequencing; among them, miR-27a-5p was significantly upregulated (P=0.000179), and miR-139-3p was significantly downregulated (P=0.000058). In the 24 patients with both CHF and PUA, qRT-PCR validated significant upregulation of miR-27a-5p (P=0.004) and downregulation of miR-139-3p (P=0.005) in serum exosomes. When combined, miR-27a-5p and miR-139-3p had a maximum area under the curve (AUC) of 0.899 (95% CI: 0812-0.987) for predicting CHF complicated by HUA. GO and KEGG enrichment analyses suggested that the differential expressions of miR-27a-5p and miR-139-3p was associated with the activation of the AMPK-mTOR signaling pathway to activate the autophagic response. We obtained the same conclusion from animal experiment.CONCLUSIONSUpregulated exosomal miR-27a-5p combined with downregulated exosomal miR-139-3p expression can serve as a novel molecular marker for diagnosis of CHF complicated by HUA, and their differential expression may promote autophagy in cardiomyocytes by activating the AMPK-mTOR signaling pathway.

01 Jan 2025·Gene

Exosomal miRNAs in patients with chronic heart failure and hyperuricemia and the underlying mechanisms

Article

Author: Huang, Xia ; Shi, Jun ; Chen, Zhiliang ; Qu, Yuan ; Gu, Ning ; Yang, Yonggang ; Cheng, Yan

Chronic heart failure (CHF) combined with hyperuricemia (HUA) is a comorbidity that is hard to diagnose by a single biomarker. Exosomal miRNAs are differentially expressed in cardiovascular diseases and are closely associated with regulating most biological functions. This study aimed to provide evidence for miRNA as a new molecular marker for precise diagnosis of the comorbidity of CHF with HUA and further analyze the potential targets of differentially expressed miRNA. This controlled study included 30 CHF patients combined with HUA (Group T) and 30 healthy volunteers (Group C). 6 peripheral blood samples from Group T and Group C were analyzed for exosomal miRNAs by high-throughput sequencing and then validated in the remaining 24 peripheral blood samples from Group T and Group C by applying real-time PCR (RT-PCR). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed using R software to predict the differential miRNAs' action targets. 42 differentially expressed miRNAs were detected (18 upregulated and 24 downregulated), in which miR-27a-5p was significantly upregulated (P<0.01), and miR-139-3p was significantly downregulated (P<0.01) in Group T. The combination of miR-27a-5p and miR-139-3p predicted the development of CHF combined with HUA with a maximum area under the curve (AUC) of 0.899 (95 % CI: 0.812-0.987, SEN=79.2 %, SPE=91.7 %, J value = 0.709). GO and KEGG enrichment analysis revealed that the differentially expressed miRNAs had a role in activating the AMPK-mTOR signaling pathway to activate the autophagic response. Collectively, our findings suggest that upregulated exosomal miR-27a-5p combined with downregulated exosomal miR-139-3p can be used as a novel molecular marker for precise diagnosis of CHF combined with HUA and enhanced autophagy by AMPK-mTOR signaling pathway may be one pathogenesis of the differentially expressed miRNAs.

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MIR139

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