2020
DOI: 10.1155/2020/7231243
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Abstract: Background. Microvascular obstruction (MVO) can result in coronary microcirculation embolism and myocardial microinfarction. Myocardial injury induced by MVO is characterized by continuous ischemia and hypoxia of cardiomyocytes. Autophagy and apoptosis are closely associated with various cardiovascular diseases. Based on our previous study, we observed a decrease in miR-30e-3p expression and an increase in Egr-1 expression in a rat coronary microembolization model. However, the specific function of miR-30e-3p … Show more

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Cited by 22 publications
(9 citation statements)
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“…MiR-320-3p can protect rat cardiomyocytes from ischemia/reperfusion (HR) injury through targeting Akt3 (Cao and Chai, 2020). MiR-30e-3p is involved in promoting cardiomyocyte autophagy and inhibiting apoptosis by regulating Egr-1 (Su et al, 2020). MiR-30b-5p exerts the suppression of fibrogenesis in Ang II-treated cardiac fibroblasts via targeting PTAFR (Zhao et al, 2020).…”
Section: Discussionmentioning
confidence: 99%
“…MiR-320-3p can protect rat cardiomyocytes from ischemia/reperfusion (HR) injury through targeting Akt3 (Cao and Chai, 2020). MiR-30e-3p is involved in promoting cardiomyocyte autophagy and inhibiting apoptosis by regulating Egr-1 (Su et al, 2020). MiR-30b-5p exerts the suppression of fibrogenesis in Ang II-treated cardiac fibroblasts via targeting PTAFR (Zhao et al, 2020).…”
Section: Discussionmentioning
confidence: 99%
“…The miR-212/miR-132 family directly targets the pro-autophagic FoxO3 transcription factor and overexpression of these miRNAs leads to an impaired autophagic response [101]; similarly, Lv et al observed upregulation of miR-302a-3p in mice undergoing ischemia/ reperfusion, and miR-302a-3p upregulation inhibits FOXO3 [102]. Intriguingly, miR-19a decreases cell apoptosis and necrosis via repression of Bim, a proapoptotic protein, and switches on autophagy in rat cardiomyocytes under hypoxia [103]; equally important, miR-30e-3p promotes cardiomyocyte autophagy and inhibits apoptosis by indirectly regulating the expression of Egr-1 (Early growth response-1), a zinc finger transcriptional protein that has been associated with cardiovascular disorders [104], in an ischemic/hypoxic environment [105]. Most recently, the inhibition of miR-17-5p was shown to inhibit myocardial autophagy through targeting STAT3 [106].…”
Section: Mirnas and Cardiomyocyte Autophagymentioning
confidence: 99%
“…It is the superiority of the aforementioned induced differentiation therapy that has made differentiation induction a research hotspot in recent years (12)(13)(14)(15). Expression of early growth response-1 (Egr-1) is a member of the early growth response protein family, which has been considered to be of great significance in a variety of physiological processes and has been extensively studied (16,17), especially in cell proliferation, angiogenesis, invasion and immune response of tumors (18,19). Egr-1 can act as a transcriptional regulator by combining the C2H2 type zinc finger with the DNA motif of the 5'-GCG(T/G)GGGCG-3' sequence.…”
Section: Mir-let-7c-3p Targeting On Egr-1 Contributes To the Committe...mentioning
confidence: 99%
“…Regardless of the methylation status of cytosine, it can bind to double-stranded target DNA and the target DNA that does not bind to cytosine is oxidized to 5-formylcytosine or 5-carboxycytosine (20,21). As it is an important part of certain signal pathways in the process of cell signal transduction, it can mediate the coupling of intracellular signal cascades and regulate the transcription and transcription of a number of downstream long-term response genes that determine cell karyotype changes (16,17). To a certain extent, the role of Egr-1 in cell proliferation and differentiation is heterogeneous, especially in normal somatic cells and malignant tumor cells.…”
Section: Mir-let-7c-3p Targeting On Egr-1 Contributes To the Committe...mentioning
confidence: 99%