scholarly journals Upregulated microRNA-210-3p improves sevoflurane-induced protective effect on ventricular remodeling in rats with myocardial infarction by inhibiting ADCY9

Author(s):  
Yahui Wu ◽  
Taofu Wang ◽  
Liang Qiao ◽  
Hongqi Lin
2021 ◽  
Author(s):  
Yahui Wu ◽  
Taofu Wang ◽  
Liang Qiao ◽  
Hongqi Lin

Abstract ObjectiveMyocardial infarction (MI) is a significant cause of death and disability, and sevoflurane (sevo) can protect myocardium in clinic. We aim to assess the effects of miR-210-3p on MI rats undergoing sevo treatment with the involvement of adenylyl cyclase type 9 (ADCY9).MethodsRat MI models were constructed by ligation of the left anterior descending and the modeled mice were respectively treated with sevo, miR-210-3p agomir/antagomir or overexpressed ADCY9. Then, miR-210-3p and ADCY9 expression, cardiac function, myocardial injury and fibrosis, and cardiomyocyte apoptosis in rats were evaluated. Target relation between miR-210-3p and ADCY9 was detected.ResultsMiR-210-3p was downregulated while ADCY9 was upregulated in MI rats. Sevo was able to promote cardiac function and attenuate myocardial injury and fibrosis, as well as cardiomyocyte apoptosis in MI rats. These effects of sevo were strengthened by miR-210-3p elevation while abolished by miR-210-3p inhibition. The role of elevated miR-210-3p in MI rats was reversed by overexpression of ADCY9.ConclusionUpregulated miR-210-3p improves sevo-induced protective effect on ventricular remodeling in rats with MI through inhibiting ADCY9.


2019 ◽  
Vol 4 (3) ◽  
pp. 120-123
Author(s):  
Ioana Cîrneală ◽  
Diana Opincariu ◽  
István Kovács ◽  
Monica Chițu ◽  
Imre Benedek

Abstract Heart failure is a clinical syndrome that appears as a consequence of a structural disease, and the most common cause of left ventricular systolic dysfunction results from myocardial ischemia. Cardiac remodeling and neuroendocrine activation are the major compensatory mechanisms in heart failure. The main objective of the study is to identify the association between serum biomarkers illustrating the extent of myocardial necrosis (highly sensitive troponin as-says), left ventricular dysfunction (NT-proBNP), and systemic inflammatory response (illustrated via serum levels of hsCRP and interleukins) during the acute phase of a myocardial infarction, and the left ventricular remodeling process at 6 months following the acute event, quantified via speckle tracking echocardiography. The study will include 400 patients diagnosed with acute myocardial infarction without signs and symptoms of heart failure at the time of enrollment that will undergo a complex clinical examination and speckle tracking echocardiography. Serum samples from the peripheral blood will be collected in order to determine the inflammatory serum biomarkers. After 6 months, patients will be divided into 2 groups according to the development of ventricular remodeling, quantified by speckle tracking echocardiography: group 1 will consist of patients with a remodeling index lower than 15%, and group 2 will consist of patients with a remodeling index higher than 15%. All clinical and imaging data obtained at the baseline will be compared between these two groups in order to determine the features associated with a higher risk of deleterious ventricular remodeling and heart failure.


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