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Last update 08 May 2025

miR-204-5p

Last update 08 May 2025

Basic Info

Synonyms-

Introduction-

Drugs associated with miR-204-5p

Salvianolic acid A

Target

miR-204-5p

Mechanism

miR-204-5p inhibitors

Active Org.

Zhejiang Chinese Medical University [+3]

Originator Org.

Chinese Academy of Medical Sciences

Active Indication

Diabetic peripheral neuropathy [+4]

Inactive Indication

Angina Pectoris

Drug Highest PhasePhase 2

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with miR-204-5p

ChiCTR2500097435

/ CompletedNot ApplicableIIT

Inhibitory effect of salvianolic acid A on platelet activation and aggregation in patients with platelet resistance

Start Date17 Oct 2023

Sponsor / Collaborator-

ITMCTR2024000668

/ CompletedNot ApplicableIIT

Salvianolic acid A inhibits the activation and aggregation of platelets in patients with acute coronary syndrome

Start Date01 Oct 2022

Sponsor / Collaborator-

CTR20213269

/ CompletedPhase 2

评估注射用丹酚酸A钠用于急性心肌梗死患者PCI术后心肌保护的有效性和安全性的随机、双盲、安慰剂对照、多中心的IIa期临床研究

[Translation] A randomized, double-blind, placebo-controlled, multicenter phase IIa clinical study to evaluate the efficacy and safety of sodium salvianolic acid A for injection in myocardial protection in patients with acute myocardial infarction after PCI

评价注射用丹酚酸A钠用于急性心肌梗死患者PCI术后心肌保护的有效性与安全性

[Translation]

To evaluate the efficacy and safety of sodium salvianolic acid A for injection in myocardial protection in patients with acute myocardial infarction after PCI

Start Date04 May 2022

Sponsor / Collaborator

Chia Tai Qingchunbao Pharmaceutical Co., Ltd.

[+1]

100 Clinical Results associated with miR-204-5p

100 Translational Medicine associated with miR-204-5p

0 Patents (Medical) associated with miR-204-5p

175

Literatures (Medical) associated with miR-204-5p

01 Jun 2025·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

CircPICALM promotes neonatal acute kidney injury triggered by hypoxia/reoxygenation via sponging microRNA-204-5p

Article

Author: Yang, Yang ; Wang, Mu-Zi ; Liu, Tian-Yu ; Zhou, Xiao-Guang ; Shi, Jia ; Pan, Jing-Jing ; Chen, Xiao-Qing

BACKGROUNDCircular RNAs (circRNAs) have been documented to regulate neonatal acute kidney injury (AKI). Based on previous RNA-sequence findings, circPICALM exhibited significantly disparate expression between AKI newborns and Controls. This study aimed to provide further insights into the regulatory mechanism of circPICALM in neonatal AKI.METHODSC57BL/6 mice born 7 days were divided into Control group and hypoxia groups (11%O₂ and 8%O₂ groups). Human tubule epithelial cells (HK-2) were stimulated with hypoxia/reoxygenation (H/R) to establish an AKI cell model. Through overexpression and knockdown techniques, the regulatory role of circPICALM in H/R-induced kidney injury was explored. Inflammatory cytokines, cell apoptosis, and oxidative stress were also detected to confirm the regulatory function of circPICALM in neonatal AKI.RESULTSRT-qPCR confirmed that circPICALM was highly expressed in the serum of AKI newborns, neonatal I/R mice and H/R-treated HK-2 cells. Functionally, circPICALM exacerbated H/R-induced HK-2 cell injury by aggravating apoptosis and mitochondrial oxidative stress, increasing the expression of inflammatory factors, including IL-6, IL-1β, and TNF-α. Conversely, inhibition of circPICALM alleviated H/R injury in the HK-2 cell line. The interaction between circPICALM and miR-204-5p was validated through RNA immunoprecipitation and luciferase assay. Finally, circPICALM functioned as a molecular sponge of miR-204-5p and promoted the upregulation of downstream IL-1β expression.CONCLUSIONCircPICALM plays a critical role in H/R-induced neonatal AKI by sponging miR-204-5p and then activating the downstream IL-1β signaling axis. The inhibition of circPICALM and subsequent suppression of pro-inflammatory factors could serve as a promising biomarker and therapeutic target for early intervention in neonatal AKI.

01 Apr 2025·Journal of Biochemical and Molecular Toxicology

M2 Macrophage‐Extracellular Vesicle‐Derived lncRNA‐NEAT1 Regulates miR‐204‐5p/RRS1‐mediated Cell Cycle to Promote the Occurrence and Development of Colorectal Cancer

Article

Author: Ma, Guorui ; Wu, Xinlin ; Bao, Zhe ; Agudamu ; Shen, Junjie ; Yang, Zhiwen

ABSTRACTColorectal cancer (CRC) is a prevalent malignancy of the digestive system. Here, we explored the role of M2 macrophage‐derived extracellular vesicles (EVs) carrying long non‐coding RNA‐nuclear paraspeckle assembly transcript 1 (lncRNA‐NEAT1) in promoting CRC progression via regulation of the miR‐204‐5p/regulator of ribosome synthesis 1 (RRS1) axis and cell cycle dynamics. Firstly, we differentiated WTHP‐1 cells into M0 and M2 macrophages and transfected M2 macrophages with sh‐NEAT1 lentivirus plasmids. EVs were isolated from M2 macrophages and administered to SW480 cells along with miR‐204‐5p inhibitors or si‐RRS1 for 24 h. M2‐EVs‐derived lncRNA‐NEAT1 enhanced CRC cell proliferation, migration, invasion, and viability while reducing apoptosis. This was accompanied by increased expression of RRS1, WEE1 G2 checkpoint kinase (WEE1), cyclin‐dependent kinase 1 (CDK1), and CyclinB1, reduced miR‐204‐5p levels, and a lower proportion of cells in the G2/M phase. Knockdown of lncRNA‐NEAT1 in M2 macrophages reversed these effects. Mechanistically, M2‐EVs‐derived lncRNA‐NEAT1 functioned as a competing endogenous RNA (ceRNA), sponging miR‐204‐5p to upregulate RRS1 expression. In summary, M2 macrophage‐derived EVs carrying lncRNA‐NEAT1 promote CRC development by modulating the miR‐204‐5p/RRS1 axis, influencing the cell cycle and apoptosis. These findings provide insights into the tumor‐promoting mechanisms of macrophage‐derived EVs in CRC.

01 Mar 2025·Diabetes, Obesity and Metabolism

Islet‐derived exosomal miR‐204 accelerates insulin resistance in skeletal muscle by suppressing sirtuin 1: An in vivo study in a mouse model of high‐fat diet–induced obesity

Article

Author: Yang, Xuehan ; Wang, Sushan ; Zhang, Meishuang ; Li, Wei ; Teng, Fei ; Lv, Xiaoyan ; Zhang, Ming ; Zhang, Ying ; Chen, Li ; Zhang, Siwei ; Han, Hao

AbstractAims: The interaction between pancreatic islets and skeletal muscle plays a pivotal role in the development of insulin resistance. The present study aimed to elucidate the impact of non‐hormonal molecules from islets on the insulin sensitivity of skeletal muscle cells.Materials and Methods:We developed a mouse model of obesity through a high‐fat diet, assessing glucose tolerance and conducting miRNA sequencing on skeletal muscle samples. An in vitro model was established by treating cells with palmitic acid, and exosomes in the supernatant were characterized using scanning electron microscopy and CD63 expression analysis. Intracellular miR‐204‐5p levels were quantified by RT‐PCR.Results: Our in vivo model demonstrated a robust correlation between miR‐204‐5p level alterations and obesity‐induced insulin resistance. Elevated fatty acid levels were observed to increase miR‐204‐5p in both skeletal muscle and islets. In cellular studies, palmitic acid increased miR‐204‐5p in MIN‐6 islet β‐cells but not in C2C12 skeletal muscle cells. Exosomes containing miR‐204‐5p, secreted by palmitic acid‐treated MIN6 cells, were identified through morphological examination, immunoblotting for the exosomal marker CD63, and intraexosomal miR‐204‐5p level measurement. C2C12 cells were shown to uptake islet‐derived miR‐204‐5p exosomes, as evidenced by the uptake of Exo‐Red labeled exosomes. TargetScan analysis identified a highly conserved binding site for miR‐204‐5p in the 3' UTR of Sirt mRNA. Functional studies indicated that miR‐204‐5p overexpression reduced glucose consumption and uptake in C2C12 cells, decreased Sirt expression, and impaired insulin signaling, as evidenced by reduced Akt phosphorylation and membrane Glut4 levels.Conclusions: Our findings reveal that miR‐204‐5p contributes to the development of insulin resistance in obesity and acts as a signaling molecule in the crosstalk between pancreatic islets and skeletal muscle.

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miR-204-5p

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