MicroRNA‐98 attenuates cardiac ischemia‐reperfusion injury through inhibiting DAPK1 expression

Zhai, Chao; Tang, Guping; Qian, Gang; Wang, Shijun; Yin, Dong; Zhang, Song

doi:10.1002/iub.1879

Cited by 21 publications

(15 citation statements)

References 35 publications

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“…Post-treatment with carvacrol also promoted an increase in the expression of the DAPK1 gene and a decrease in the enzyme PPP2R2A ( Li et al, 2019 ). DAPK1 is a serine/threonine kinase, a tumor suppressor protein that promotes apoptosis ( Agodi et al, 2015 ; Zhai et al, 2019 ), while PPP2R2A, a regulatory subunit of protein phosphatase 2A (PP2A), controls the pathway of AKT signaling associated with tumor growth ( Wang et al, 2016 ; Zeng et al, 2016 ). In fact, both may be involved in a possible antitumor mechanism of carvacrol, but it is still not very clear, requiring further studies ( Li et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Antitumor Effects of Carvacrol and Thymol: A Systematic Review

et al. 2021

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Background: It is estimated that one in five people worldwide faces a diagnosis of a malignant neoplasm during their lifetime. Carvacrol and its isomer, thymol, are natural compounds that act against several diseases, including cancer. Thus, this systematic review aimed to examine and synthesize the knowledge on the antitumor effects of carvacrol and thymol.Methods: A systematic literature search was carried out in the PubMed, Web of Science, Scopus and Lilacs databases in April 2020 (updated in March 2021) based on the PRISMA 2020 guidelines. The following combination of health descriptors, MeSH terms and their synonyms were used: carvacrol, thymol, antitumor, antineoplastic, anticancer, cytotoxicity, apoptosis, cell proliferation, in vitro and in vivo. To assess the risk of bias in in vivo studies, the SYRCLE Risk of Bias tool was used, and for in vitro studies, a modified version was used.Results: A total of 1,170 records were identified, with 77 meeting the established criteria. The studies were published between 2003 and 2021, with 69 being in vitro and 10 in vivo. Forty-three used carvacrol, 19 thymol, and 15 studies tested both monoterpenes. It was attested that carvacrol and thymol induced apoptosis, cytotoxicity, cell cycle arrest, antimetastatic activity, and also displayed different antiproliferative effects and inhibition of signaling pathways (MAPKs and PI3K/AKT/mTOR).Conclusions: Carvacrol and thymol exhibited antitumor and antiproliferative activity through several signaling pathways. In vitro, carvacrol appears to be more potent than thymol. However, further in vivo studies with robust methodology are required to define a standard and safe dose, determine their toxic or side effects, and clarify its exact mechanisms of action.This systematic review was registered in the PROSPERO database (CRD42020176736) and the protocol is available at https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=176736.

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Section: Discussionmentioning

confidence: 99%

Antitumor Effects of Carvacrol and Thymol: A Systematic Review

et al. 2021

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“…It was found that the inhibition of miR‐1 may have protective effects on myocardial I/R injury . According to recent reports, miR‐98 expression was downregulated in cardiomyocytes undergoing H/R . Zhu et al hold the view that miR‐499 protected the rat heart against I/R injury through inhibiting apoptosis .…”

Section: Introductionmentioning

confidence: 99%

“…10 According to recent reports, miR-98 expression was downregulated in cardiomyocytes undergoing H/R. 11 Zhu et al hold the view that miR-499 protected the rat heart against I/R injury through inhibiting apoptosis. 12 So miRNAs may be proposed as diagnostic tools and novel biomarkers for cardiomyocyte.…”

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confidence: 99%

MiR‐27 alleviates myocardial cell damage induced by hypoxia/reoxygenation via targeting TGFBR1 and inhibiting NF‐κB pathway

Zhang

2019

The Kaohsiung J of Med Scie

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MiR‐27 prevents atherosclerosis by inhibiting inflammatory responses induced by lipoprotein lipase. Overexpression of miR‐27b attenuates angiotensin‐induced atrial fibrosis. Nevertheless, studies have rarely investigated on the effect of miR‐27 in cardiomyocyte injury. H9c2 cells were transfected with miR‐27 mimic/inhibitor. Then the cell proliferation was tested by MTT assay and the cell apoptosis was detected by flow cytometry. The luciferase activity assay was utilized to analyze the relationship between miR‐27 and TGFBR1. Quantificational real‐time polymerase chain reaction and western blot were utilized to detect the cardiomyocyte differentiation marker and nuclear factor kappa B (NF‐κB) pathway. Our outcomes demonstrated that miR‐27 expression was downregulated cardiomyocyte injury subjected to hypoxia/reoxygenation (H/R). Additionally, overexpression of miR‐27 could significantly alleviate cardiomyocyte injury by regulating cell activity and apoptosis. The luciferase activity assay confirmed that transforming growth factor ß receptor 1 (TGFBR1) is a direct hallmark of miR‐27. Besides, overexpression of miR‐27 promoted the expression of TGFBR1 in H/R model. After transfection with miR‐27 mimic/inhibitor, the expression of NF‐κB pathway‐related proteins was decreased/increased. Taken together, our data manifested that miR‐27 repressed cardiomyocyte injury induced by H/R via mediating TGFBR1 and inhibiting NF‐κB signaling pathway. Furthermore, miR‐27/ TGFBR1 might be utilized as hopeful biomarkers for myocardial ischemia diagnosis and treatment.

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“…Numerous miRNAs had been reported to be up-or down-regulated in patients with myocardial ischemia/reperfusion injury (Table 1). Among them, MiR-22, miR-134, miR-135a, miR-203, miR-144, miR-98, miR-18a, miR-210, miR-340-5p, miR-374a-5p, and miR-1192 exert protective effects in cardiovascular ischemic injury through downregulating their target genes [37,41,56,77,79,112,160,163,175,183,184]. On the other hand, a specific set of miRNAs has been linked to cardiac dysfunctions in varied cardiac injury models.…”

Section: Roles Of Mirnasmentioning

confidence: 99%

Pathophysiological implications of hypoxia in human diseases

et al. 2020

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Oxygen is essentially required by most eukaryotic organisms as a scavenger to remove harmful electron and hydrogen ions or as a critical substrate to ensure the proper execution of enzymatic reactions. All nucleated cells can sense oxygen concentration and respond to reduced oxygen availability (hypoxia). When oxygen delivery is disrupted or reduced, the organisms will develop numerous adaptive mechanisms to facilitate cells survived in the hypoxic condition. Normally, such hypoxic response will cease when oxygen level is restored. However, the situation becomes complicated if hypoxic stress persists (chronic hypoxia) or cyclic normoxia-hypoxia phenomenon occurs (intermittent hypoxia). A series of chain reaction-like gene expression cascade, termed hypoxia-mediated gene regulatory network, will be initiated under such prolonged or intermittent hypoxic conditions and subsequently leads to alteration of cellular function and/or behaviors. As a result, irreversible processes occur that may cause physiological disorder or even pathological consequences. A growing body of evidence implicates that hypoxia plays critical roles in the pathogenesis of major causes of mortality including cancer, myocardial ischemia, metabolic diseases, and chronic heart and kidney diseases, and in reproductive diseases such as preeclampsia and endometriosis. This review article will summarize current understandings regarding the molecular mechanism of hypoxia in these common and important diseases.

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MicroRNA‐98 attenuates cardiac ischemia‐reperfusion injury through inhibiting DAPK1 expression

Cited by 21 publications

References 35 publications

Antitumor Effects of Carvacrol and Thymol: A Systematic Review

Antitumor Effects of Carvacrol and Thymol: A Systematic Review

MiR‐27 alleviates myocardial cell damage induced by hypoxia/reoxygenation via targeting TGFBR1 and inhibiting NF‐κB pathway

Pathophysiological implications of hypoxia in human diseases

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