The circular RNA TLK1 exacerbates myocardial ischemia/reperfusion injury via targeting miR-214/RIPK1 through TNF signaling pathway

Song, Yinsen; Zhao, Liang; Wang, Baocai; Sun, Jun; Hu, Junlong; Zhu, Xiliang; Zhao, Jian; Zheng, Daokuo; Ge, Zhenwei

doi:10.1016/j.freeradbiomed.2020.05.013

Cited by 53 publications

(36 citation statements)

References 31 publications

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“…TNF is a critical cytokine that induces a wide range of intracellular signal pathways including cell survival, immunity, apoptosis, and inflammation (Ting & Bertrand, 2016; Wallach, 2016). Inflammation associated with the TNF signaling pathway is critical during myocardial I/R as well as in the pathology of a wide range of diseases (Shao et al, 2019; Song et al, 2020; Williams, Huang, & Randolph, 2019; Yang et al, 2020). Suppressing inflammation by targeting the transcription factor nuclear factor‐κB helps us to prevent MI and other diseases including colitis, cystic fibrosis, arthritis, and atopic dermatitis (Giridharan & Srinivasan, 2018).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of cathepsin S attenuates myocardial ischemia/reperfusion injury by suppressing inflammation and apoptosis

Peng

Liu

Yan

et al. 2020

Journal Cellular Physiology

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Myocardial ischemia/reperfusion (I/R) injury leads to high mortality and morbidity due to the incomplete understanding of the underlying mechanism and the consequent lack of effective therapy. The present study revealed and validated key candidate genes in relation to inflammation and apoptosis pathways underlying myocardial I/R injury. Cathepsin S was identified as the top hub protein based on the protein-protein interaction analysis, and, thus, its role during myocardial I/R injury was further investigated. Myocardial I/R in mice resulted in significantly increased levels of myocardial injury biomarkers (cardiac troponin I, lactic dehydrogenase, and creatinine kinase-MB) and inflammatory cytokines (interleukin-1β [IL-1β], IL-6, and tumor necrosis factor-α), elevated apoptosis rate, and upregulated protein expression of cleaved caspase-8, cleaved caspase-3, and cleaved poly ADP-ribose polymerase. These abovementioned changes were blocked by two different selective cathepsin S inhibitors, LY3000328 or MIV-247. Moreover, Kaplan-Meier survival plot showed that cathepsin S inhibition improved 21-day survival rate following myocardial I/R injury. This study demonstrated that the inhibition of cathepsin S alleviated myocardial I/R-induced injury by suppressing inflammation and apoptosis, which may be used in clinical applications of cardioprotection.

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Section: Discussionmentioning

confidence: 99%

Inhibition of cathepsin S attenuates myocardial ischemia/reperfusion injury by suppressing inflammation and apoptosis

Peng

Liu

Yan

et al. 2020

Journal Cellular Physiology

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“…Another study demonstrated that circ-TLK1 is overexpressed in renal cell carcinoma and that downregulation of circ-TLK1 significantly depressed cell proliferation, migration and invasion of renal cell carcinoma in vitro and in vivo [226]. circ-TLK1 upregulation was also found in MIRI mice; low levels of circ-TLK1 markedly decreased the number of apoptotic cardiomyocytes and improved the cardiac function in these animals [222].…”

Section: Mirnas In Mirimentioning

confidence: 96%

“…In this section we will summarize several circRNA-miRNA-mRNA pathways in MIRI, including circ-TLK1/miR-214/RIPK1, circ-100338/miR-200a-3p/FUS and circ-0068566/miR-6322/PARP2 (Table 6). circ-TLK1 was found to be elevated in MIRI mice, where its downregulation effectively decreased the apoptotic cardiomyocytes and attenuated the pathogenesis of MIRI [222]. miR-214 is a downstream effector which reverses circ-TLK1-mediated destructive effects in MIRI by directly targeting RIPK1 via binding to its 3 UTR [222].…”

Section: Mirnas In Mirimentioning

confidence: 99%

“…miR-214 is a downstream effector which reverses circ-TLK1-mediated destructive effects in MIRI by directly targeting RIPK1 via binding to its 3 UTR [222]. RIPK1 overexpression results in cardiac dysfunctions, increased infarct area and cell apoptosis; it abolishes the protective effects exerted by miR-214, indicating the important action of the circ-TLK1/miR-214/RIPK1 regulatory network involved in MIRI [222].…”

Section: Mirnas In Mirimentioning

confidence: 99%

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Roles of Noncoding RNAs in the Initiation and Progression of Myocardial Ischemia-Reperfusion Injury

et al. 2021

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The morbidity and mortality of myocardial ischemia reperfusion injury (MIRI) have increased in modern society. Noncoding RNAs (ncRNAs), including lncRNAs, circRNAs, piRNAs and miRNAs, have been reported in a variety of studies to be involved in pathological initiation and developments of MIRI. Hence this review focuses on the current research regarding these ncRNAs in MIRI. We comprehensively introduce the important features of lncRNAs, circRNAs, piRNA and miRNAs and then summarize the published studies of ncRNAs in MIRI. A clarification of lncRNA–miRNA–mRNA, lncRNA–transcription factor–mRNA and circRNA–miRNA–mRNA axes in MIRI follows, to further elucidate the crucial roles of ncRNAs in MIRI. Bioinformatics analysis has revealed the biological correlation of mRNAs with MIRI. We provide a comprehensive perspective for the roles of these ncRNAs and their related networks in MIRI, providing a theoretical basis for preclinical and clinical studies on ncRNA-based gene therapy for MIRI treatment.

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“…Circular RNAs are a class of non‐coding RNAs that are involved in the development of vascular diseases 5,6 . Circular circTLK1 deteriorated myocardial ischaemia/reperfusion injury via regulating the TNF signalling pathway 7 . CircRNAs are abundant in the brain tissues 8 and have been implicated in neurological functions 9 and acute ischaemic stroke 6 .…”

Section: Introductionmentioning

confidence: 99%

Circular RNA circCCDC9 alleviates ischaemic stroke ischaemia/reperfusion injury via the Notch pathway

Zhang

et al. 2020

J Cellular Molecular Medi

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Stroke is a leading cause of mortality and disability globally. 1-3 There are more than two million ischaemic stroke cases in adults aged 18-50 years annually. 3 Modifiable lifestyle risk factors, including smoking, physical activity, diet, alcohol consumption and weight, could cut down the risk of stroke. For patients with ischaemic stroke, the most effective and frequently used treatment would be early reperfusion with intravenous thrombolysis and thrombectomy. However, these treatments are limited by a narrow time window and side effects. 4 Given this situation, there is an urgent need to develop novel treatments for patients with ischaemic stroke. Circular RNAs are a class of non-coding RNAs that are involved in the development of vascular diseases. 5,6 Circular circTLK1 deteriorated myocardial ischaemia/reperfusion injury via regulating the TNF signalling pathway. 7 CircRNAs are abundant in the brain tissues 8 and have been implicated in neurological functions 9 and acute ischaemic stroke. 6 A total of 521 differentially expressed circRNAs were found in the peripheral blood mononuclear cells of patients with acute ischaemic stroke compared to healthy controls, which suggested that circRNAs were potential markers for the diagnosis

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The circular RNA TLK1 exacerbates myocardial ischemia/reperfusion injury via targeting miR-214/RIPK1 through TNF signaling pathway

Cited by 53 publications

References 31 publications

Inhibition of cathepsin S attenuates myocardial ischemia/reperfusion injury by suppressing inflammation and apoptosis

Inhibition of cathepsin S attenuates myocardial ischemia/reperfusion injury by suppressing inflammation and apoptosis

Roles of Noncoding RNAs in the Initiation and Progression of Myocardial Ischemia-Reperfusion Injury

Circular RNA circCCDC9 alleviates ischaemic stroke ischaemia/reperfusion injury via the Notch pathway

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