How to Bail Out Patients with Severe Acute Myocardial Infarction

Toma, Yuichiro

doi:10.1016/j.hfc.2019.12.004

Cited by 1 publication

(2 citation statements)

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“…The H9c2 cells were inoculated into 96 well plates, and the number of cells per well was 5×10 3 . The cells were transfected after being cultured in a constant temperature incubator for 24 h. After 48 h of transfection, the cells were treated with H 2 O 2 .…”

Section: Mttmentioning

confidence: 99%

“…The incidence and mortality rates of MI are increasing gradually. It can cause the increase of oxygen free radicals and calcium overload of cardiomyocytes, aggravate cardiomyocyte apoptosis and necrosis, and its clinical manifestations are arrhythmia, expansion of MI area, deterioration of cardiac function, and ventricular remodeling (2,3). Cardiomyocyte apoptosis, inflammation and cytokines are involved in a series of pathological changes of ventricular remodeling and heart failure after Original Article MiR-223-3p affects myocardial inflammation and apoptosis following myocardial infarction via targeting FBXW7 MI, which lead to disease progression and poor prognosis in patients with MI (4).…”

Section: Introductionmentioning

confidence: 99%

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MiR-223-3p affects myocardial inflammation and apoptosis following myocardial infarction via targeting FBXW7

et al. 2022

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Background: Myocardial infarction (MI) is one of the main causes of disability and death in the world, leading to myocarditis and cardiomyocyte apoptosis. Studies have shown that microRNA (miRNA) is involved in myocarditis and apoptosis. The main purpose of this study was to explore the regulatory mechanism of miR-223-3p on myocarditis and apoptosis after MI. Methods: We cultured H9c2 cells and detected the expression of miR-223-3p in cells treated with different concentrations of H 2 O 2 . Sprague Dawley (SD) rats were fed with normal diet, constructed an MI model and detect the expression of miR-223-3p in heart tissue. Overexpression or inhibition of miR-223-3p was conducted in MI model cells in vitro, and the contents of the inflammatory factors tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10) in cell supernatant were detected by enzymelinked immunosorbent assay (ELISA). Cell apoptosis was detected by flow cytometry. Luciferase activity assay was used to detect the targeting relationship between miR-223-3p and FBXW7, and the expression of FBXW7 in cells was also detected. Overexpression of miR-223-3p was performed in MI rats to detect the expression of inflammatory factors, FBXW7, and apoptosis in rat cardiac tissue. Results: The expression of miR-223-3p was down regulated in MI models established in vitro and in vivo. Overexpression of miR-223-3p can inhibit inflammatory response and apoptosis in H9c2 cells and cardiac tissues. It was revealed that miR-223-3p can inhibit the expression of FBXW7, reduce myocarditis and apoptosis after MI, and improve cardiac function. Conclusions: It is possible that miR-223-3p reduces myocarditis and apoptosis after MI and improves cardiac function by targeted inhibition of FBXW7 expression.

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Section: Mttmentioning

confidence: 99%