LncRNA MIAT Promotes Inflammation and Oxidative Stress in Sepsis-Induced Cardiac Injury by Targeting miR-330-5p/TRAF6/NF-κB Axis

Xing, Pengcheng; An, Peng; Hu, Guoyong; Wang, Donglian; Zhou, Minjie

doi:10.1007/s10528-020-09976-9

Cited by 64 publications

(46 citation statements)

References 33 publications

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“…For example, Xing et al indicated that lncRNA MIAT activated the NF-κB signaling pathway through the miR-330-5p/TRAF6 axis to promote inflammation and oxidative stress in LPS-induced septic cardiomyopathy. 37 Besides, studies by Chen et al 38 and Li et al 39 showed that silencing lncRNA MIAT could suppress the activity of NF-κB by directly inhibiting the nuclear transport of NF-κB-p65. Through searching StarBase v2.0, we found that lncRNA MIAT might interact with other molecules, including Nfe2l1 and NF-Y, which were reported to be closely related to NF-κB pathway.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: LncRNA MIAT regulated by selenium and T-2 toxin increases NF-κB-p65 activation, promoting the progress of Kashin-Beck Disease

Shi

Zhang

et al. 2020

Hum Exp Toxicol

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LncRNA myocardial infarction associated transcript (MIAT) has been shown to be involved in osteoarthritis (OA), but its role in Kashin-Beck Disease (KBD) has rarely been reported. In this study, rats were administered with low selenium and/or T-2 toxin for 4 weeks to establish a KBD animal model. The serum selenium level, TNF-α and IL-1β contents, phosphorylated p65 (p-p65) and MIAT expression were increased in each intervention group. Next, we isolated the primary epiphyseal chondrocytes, and found that selenium treatment reversed the effects of T-2 toxin on chondrocyte injury, p-p65 and MIAT expression. In addition, MIAT overexpression or T-2 toxin treatment led to increased cell death, apoptosis, inflammation, NF-κB-p65 pathway activation and MIAT expression, which was rescued by selenium treatment or MIAT siRNA transfection. Our results suggested that lncRNA MIAT regulated by selenium and T-2 toxin increased the activation of NF-κB-p65, thus being involved in the progress of KBD. [Formula: see text]

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Section: Discussionmentioning

confidence: 99%

RETRACTED: LncRNA MIAT regulated by selenium and T-2 toxin increases NF-κB-p65 activation, promoting the progress of Kashin-Beck Disease

Shi

Zhang

et al. 2020

Hum Exp Toxicol

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“…MiR-144-3p seemed to be involved in apoptosis and inflammation in myocardial cells via the NF-kB pathway. Xing et al investigated the role of lncRNA myocardial infarction associated transcript (MIAT) in sepsis-induced myocardial injury [ 76 ]. MIAT appeared to be a down-regulator of miR-330-5p.…”

Section: Resultsmentioning

confidence: 99%

“…NF-kB proteins are also implicated in sepsis and SIRS [ 92 , 93 ]. Therefore, it is not surprising that miRNAs implicated in sepsis myocardial damage regulate, directly or indirectly, some NF-kB-mediated pathways involved in cardiac dysfunction during sepsis [ 39 , 45 , 59 , 75 , 76 ]. Some studies suggest that inflammation and infections could have a role in atherosclerotic plaque development and coronary heart disease (CHD) [ 94 , 95 ].…”

Section: Discussionmentioning

confidence: 99%

MicroRNAs and Sepsis-Induced Cardiac Dysfunction: A Systematic Review

Manetti

Maiese

Paolo

et al. 2020

IJMS

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Sepsis is a severe condition characterized by systemic inflammation. One of the most involved organs in sepsis is the heart. On the other hand, heart failure and dysfunction are some of the most leading causes of death in septic patients. miRNAs are short single-strand non-coding ribonucleic acids involved in the regulation of gene expression on a post-transcriptional phase, which means they are a part of the epigenetic process. Recently, researchers have found that miRNA expression in tissues and blood differs depending on different conditions. Because of this property, their use as serum sepsis biomarkers has also been explored. A narrative review is carried out to gather and summarize what is known about miRNAs’ influence on cardiac dysfunction during sepsis. When reviewing the literature, we found at least 77 miRNAs involved in cardiac inflammation and dysfunction during sepsis. In the future, miRNAs may be used as early sepsis-induced cardiac dysfunction biomarkers or as new drug targets. This could help clinicians to early detect, prevent, and treat cardiac damage. The potential role of miRNAs as new diagnostic tools and therapeutic strategies worth deepening the complex network between non-coding RNA and biological pathways. Additional studies are needed to further investigate their role in sepsis-induced myocardium injury.

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“…suggested that lncRNA MIAT could promote inflammation response as well as oxidative stress in LPS-induced HL-1 cells. At the molecular level, lncRNA MIAT could target against miR-339-5p to activate TRAF6/NF-κB axis in vitro ( Xing et al., 2020 ). These studies indicate that lncRNAs participate in sepsis-induced heart dysfunction by regulating multiple pathways; however, more studies are needed to verify their clinical value.…”

Section: Role Of Lncrnas In Sepsis-induced Organ Dysfunctionsmentioning

confidence: 99%

Long Noncoding RNA: Regulatory Mechanisms and Therapeutic Potential in Sepsis

Wang

Yang

Wen

et al. 2021

Front. Cell. Infect. Microbiol.

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Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection and is characterized by a hyperinflammatory state accompanied by immunosuppression. Long noncoding RNAs (lncRNAs) are noncoding RNAs longer than 200 nucleotides and have important roles in mediating various biological processes. Recently, lncRNAs were found to exert both promotive and inhibitory immune functions in sepsis, thus participating in sepsis regulation. Additionally, several studies have revealed that lncRNAs are involved in sepsis-induced organ dysfunctions, including cardiovascular dysfunction, acute lung injury, and acute kidney injury. Considering the lack of effective biomarkers for early identification and specific treatment for sepsis, lncRNAs may be promising biomarkers and even targets for sepsis therapies. This review systematically highlights the recent advances regarding the roles of lncRNAs in sepsis and sheds light on their use as potential biomarkers and treatment targets for sepsis.

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LncRNA MIAT Promotes Inflammation and Oxidative Stress in Sepsis-Induced Cardiac Injury by Targeting miR-330-5p/TRAF6/NF-κB Axis

Cited by 64 publications

References 33 publications

RETRACTED: LncRNA MIAT regulated by selenium and T-2 toxin increases NF-κB-p65 activation, promoting the progress of Kashin-Beck Disease

RETRACTED: LncRNA MIAT regulated by selenium and T-2 toxin increases NF-κB-p65 activation, promoting the progress of Kashin-Beck Disease

MicroRNAs and Sepsis-Induced Cardiac Dysfunction: A Systematic Review

Long Noncoding RNA: Regulatory Mechanisms and Therapeutic Potential in Sepsis

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