Local Intracoronary Fibrinolysis in Acute Myocardial Infarction of Ectatic Coronary Arteries in the Post-Abciximab Era

Unzué, Leire; Garcı́a, Eulogio; Teijeiro, Rodrigo; Ginestal, Carmen; Fuertes, Beatriz; Pastor, Ana; Zorita, Blanca; Rodrigo, Francisco José Rodríguez; Osende, Julio I.; Parra, Francisco Javier; Moreno, Leire

doi:10.1016/j.carrev.2021.01.005

Cited by 3 publications

(2 citation statements)

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“…AMI is one of the important diseases that seriously endanger human health and threaten human life in clinical practice 20 . Studies have shown that the morphology, structure, and function of the heart are severely damaged after AMI 21–23 . And exercise can improve the morphology and structure and enhance the function of the heart after MI.…”

Section: Discussionmentioning

confidence: 99%

“…20 Studies have shown that the morphology, structure, and function of the heart are severely damaged after AMI. [21][22][23] And exercise can improve the morphology and structure and enhance the function of the heart after MI. LncRNA and miRNA can play their roles by regulating cardiomyocyte inflammation, fibrosis, autophagy, and neovascularization.…”

Section: Discussionmentioning

confidence: 99%

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Long noncoding RNA CASC2 protect ROS‐induced oxidative stress in myocardial infarction by miR‐18a/SIRT2

Ying

Tang

Zhang

et al. 2021

Biotech and App Biochem

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We aimed to investigate the function and its possible mechanisms of long noncoding RNA (lncRNA) in acute myocardial infarction (AMI) model. Patients with AMI and normal volunteers were selected from our hospital. Sprague-Dawley rats were induced into in vivo model of AMI. H9c2 cells were treated with H 2 O 2 to generate injury model. A significantly lower serum gene expression of lncRNA CASC2 was detected. In rat models of AMI, lncRNA CASC2 gene expressions in heart tissue of mice with AMI were decreased. In in vitro model, downregulation of lncRNA CASC2 increased reactive oxygen species (ROS)-induced oxidative stress; lncRNA CASC2 induced NADPH oxidase (NOX-2) expression and suppressed miR-18a expression; MiR-18a promoted ROS-induced oxidative stress; downregulation of miR-18a decreased ROS-induced oxidative stress. The inhibition of miR-18a reversed the effects of CASC2 downregulation on ROS-induced oxidative stress in in vitro model of AMI. The activation of miR-18a reversed the effects of CASC2 on ROS-induced oxidative stress in in vitro model of AMI. These data for the first time suggest that lncRNA CASC2 have better protective effects on AMI, which could reduce oxidative stress through their carried miR-18a and subsequently downregulating the SIRT2/ROS pathway.

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Section: Discussionmentioning

confidence: 99%