Circ_0001084/miR-181c-5p/PTPN4 Axis Mitigates Cardiomyocyte Injury by Modulating the TLR4/NF-κB Pathway: Insights into Therapeutic Potential for Myocardial Reperfusion Injury
Haihong Deng,1,* Qisen Fan,2,* Lichao Huang,1 Wenbo Ouyang,1 Wendian Zhu3 1Department of Anesthesiology, The First People’s Hospital of Zhaoqing, Zhaoqing City, Guangdong Province, People’s Republic of China; 2Department of Anesthesiology, The First Affiliated Hospital of Guangzhou M...
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Dove Medical Press
2025-01-01
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author | Deng H Fan Q Huang L Ouyang W Zhu W |
author_facet | Deng H Fan Q Huang L Ouyang W Zhu W |
author_sort | Deng H |
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description | Haihong Deng,1,* Qisen Fan,2,* Lichao Huang,1 Wenbo Ouyang,1 Wendian Zhu3 1Department of Anesthesiology, The First People’s Hospital of Zhaoqing, Zhaoqing City, Guangdong Province, People’s Republic of China; 2Department of Anesthesiology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou City, Guangdong Province, People’s Republic of China; 3Department of Hepatobiliary Surgery, The First People’s Hospital of Zhaoqing, Zhaoqing City, Guangdong Province, People’s Republic of China*These authors contributed equally to this workCorrespondence: Wendian Zhu, Department of Hepatobiliary Surgery, The First People’s Hospital of Zhaoqing, NO. 9 Donggang East Road, Duanzhou District, Zhaoqing City, Guangdong Province, People’s Republic of China, Email Zq2860676@163.comBackground: Myocardial ischemia/reperfusion (I/R) injury significantly impacts the recovery of ischemic heart disease patients. Non-coding RNAs, including miRNAs, have been increasingly recognized for their roles in regulating cardiomyocyte responses to hypoxia/reoxygenation (H/R) injury. miR-181c-5p, in particular, has been implicated in inflammatory and apoptotic processes, suggesting its potential involvement in exacerbating cellular damage.Methods: This study combined bioinformatic and experimental techniques to investigate myocardial injury. Gene expression data from the GEO database were analyzed, and HL-1 cardiomyocytes were used in a hypoxia/reoxygenation model to mimic reperfusion injury. Various molecular techniques have been applied to explore the underlying mechanisms, while statistical analyses have identified potential biomarkers and therapeutic targets.Results: This study revealed significant upregulation of miR-181c-5p in cardiomyocyte H/R injury models, which inversely affected PTPN4 expression and activated the TLR4/NF-κB signaling pathway. Overexpression of PTPN4 inhibited this pathway. Notably, circ_0001084 was identified as absorbing miR-181c-5p, reducing its interaction with PTPN4 and subsequent pathway activation. This suggests a novel therapeutic pathway for myocardial I/R injury treatment, highlighting the interplay between non-coding RNAs and cellular stress responses.Conclusion: circ_0001084 acts as a competing endogenous RNA for miR-181c-5p, enhancing PTPN4 expression and inhibiting the TLR4/NF-κB signaling pathway. These findings offer insights into the molecular mechanisms of myocardial I/R injury and potential therapeutic targets in ischemic heart disease.Keywords: Myocardial, Circ_0001084/miR-181c-5p/PTPN4 axis, Cardiomyocyte hypoxia, Reoxygenation, TLR4/NF-κB pathway |
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spelling | doaj-art-0f19a1fba695466186a1786195e9786b2025-01-23T18:50:32ZengDove Medical PressJournal of Inflammation Research1178-70312025-01-01Volume 181033105199481Circ_0001084/miR-181c-5p/PTPN4 Axis Mitigates Cardiomyocyte Injury by Modulating the TLR4/NF-κB Pathway: Insights into Therapeutic Potential for Myocardial Reperfusion InjuryDeng HFan QHuang LOuyang WZhu WHaihong Deng,1,* Qisen Fan,2,* Lichao Huang,1 Wenbo Ouyang,1 Wendian Zhu3 1Department of Anesthesiology, The First People’s Hospital of Zhaoqing, Zhaoqing City, Guangdong Province, People’s Republic of China; 2Department of Anesthesiology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou City, Guangdong Province, People’s Republic of China; 3Department of Hepatobiliary Surgery, The First People’s Hospital of Zhaoqing, Zhaoqing City, Guangdong Province, People’s Republic of China*These authors contributed equally to this workCorrespondence: Wendian Zhu, Department of Hepatobiliary Surgery, The First People’s Hospital of Zhaoqing, NO. 9 Donggang East Road, Duanzhou District, Zhaoqing City, Guangdong Province, People’s Republic of China, Email Zq2860676@163.comBackground: Myocardial ischemia/reperfusion (I/R) injury significantly impacts the recovery of ischemic heart disease patients. Non-coding RNAs, including miRNAs, have been increasingly recognized for their roles in regulating cardiomyocyte responses to hypoxia/reoxygenation (H/R) injury. miR-181c-5p, in particular, has been implicated in inflammatory and apoptotic processes, suggesting its potential involvement in exacerbating cellular damage.Methods: This study combined bioinformatic and experimental techniques to investigate myocardial injury. Gene expression data from the GEO database were analyzed, and HL-1 cardiomyocytes were used in a hypoxia/reoxygenation model to mimic reperfusion injury. Various molecular techniques have been applied to explore the underlying mechanisms, while statistical analyses have identified potential biomarkers and therapeutic targets.Results: This study revealed significant upregulation of miR-181c-5p in cardiomyocyte H/R injury models, which inversely affected PTPN4 expression and activated the TLR4/NF-κB signaling pathway. Overexpression of PTPN4 inhibited this pathway. Notably, circ_0001084 was identified as absorbing miR-181c-5p, reducing its interaction with PTPN4 and subsequent pathway activation. This suggests a novel therapeutic pathway for myocardial I/R injury treatment, highlighting the interplay between non-coding RNAs and cellular stress responses.Conclusion: circ_0001084 acts as a competing endogenous RNA for miR-181c-5p, enhancing PTPN4 expression and inhibiting the TLR4/NF-κB signaling pathway. These findings offer insights into the molecular mechanisms of myocardial I/R injury and potential therapeutic targets in ischemic heart disease.Keywords: Myocardial, Circ_0001084/miR-181c-5p/PTPN4 axis, Cardiomyocyte hypoxia, Reoxygenation, TLR4/NF-κB pathwayhttps://www.dovepress.com/circ0001084mir-181c-5pptpn4-axis-mitigates-cardiomyocyte-injury-by-mod-peer-reviewed-fulltext-article-JIRmyocardialcirc_0001084/mir-181c-5p/ptpn4 axiscardiomyocyte hypoxiareoxygenationtlr4/nf-κb pathway |
spellingShingle | Deng H Fan Q Huang L Ouyang W Zhu W Circ_0001084/miR-181c-5p/PTPN4 Axis Mitigates Cardiomyocyte Injury by Modulating the TLR4/NF-κB Pathway: Insights into Therapeutic Potential for Myocardial Reperfusion Injury Journal of Inflammation Research myocardial circ_0001084/mir-181c-5p/ptpn4 axis cardiomyocyte hypoxia reoxygenation tlr4/nf-κb pathway |
title | Circ_0001084/miR-181c-5p/PTPN4 Axis Mitigates Cardiomyocyte Injury by Modulating the TLR4/NF-κB Pathway: Insights into Therapeutic Potential for Myocardial Reperfusion Injury |
title_full | Circ_0001084/miR-181c-5p/PTPN4 Axis Mitigates Cardiomyocyte Injury by Modulating the TLR4/NF-κB Pathway: Insights into Therapeutic Potential for Myocardial Reperfusion Injury |
title_fullStr | Circ_0001084/miR-181c-5p/PTPN4 Axis Mitigates Cardiomyocyte Injury by Modulating the TLR4/NF-κB Pathway: Insights into Therapeutic Potential for Myocardial Reperfusion Injury |
title_full_unstemmed | Circ_0001084/miR-181c-5p/PTPN4 Axis Mitigates Cardiomyocyte Injury by Modulating the TLR4/NF-κB Pathway: Insights into Therapeutic Potential for Myocardial Reperfusion Injury |
title_short | Circ_0001084/miR-181c-5p/PTPN4 Axis Mitigates Cardiomyocyte Injury by Modulating the TLR4/NF-κB Pathway: Insights into Therapeutic Potential for Myocardial Reperfusion Injury |
title_sort | circ 0001084 mir 181c 5p ptpn4 axis mitigates cardiomyocyte injury by modulating the tlr4 nf kappa b pathway insights into therapeutic potential for myocardial reperfusion injury |
topic | myocardial circ_0001084/mir-181c-5p/ptpn4 axis cardiomyocyte hypoxia reoxygenation tlr4/nf-κb pathway |
url | https://www.dovepress.com/circ0001084mir-181c-5pptpn4-axis-mitigates-cardiomyocyte-injury-by-mod-peer-reviewed-fulltext-article-JIR |
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