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Tytuł pozycji:

The Therapeutic Potential of Blocking Galectin-3 Expression in Acute Myocardial Infarction and Mitigating Inflammation of Infarct Region: A Clinical Outcome-Based Translational Study.

Tytuł:
The Therapeutic Potential of Blocking Galectin-3 Expression in Acute Myocardial Infarction and Mitigating Inflammation of Infarct Region: A Clinical Outcome-Based Translational Study.
Autorzy:
Mosleh, Wassim
Chaudhari, Milind R.
Sonkawade, Swati
Mahajan, Supriya
Khalil, Charl
Frodey, Kevin
Shah, Tanvi
Dahal, Suraj
Karki, Roshan
Katkar, Rujuta
Blankesteijn, W. Matthijs
Page, Brian
Pokharel, Saraswati
Kim, Minhyung
Sharma, Umesh C.
Temat:
GALECTINS
MYOCARDIAL infarction
CARDIOMYOPATHIES
KNOCK-out reactions
LIGATION reactions
MORTALITY
Źródło:
Biomarker Insights; Jan-Dec2018, Issue 13, p1-1, 1p
Czasopismo naukowe
Introduction: Increased galectin-3 is associated with ischemic cardiomyopathy, although its role in early remodeling post-myocardial infarction (MI) has not been fully elucidated. There are no data demonstrating that blocking galectin-3 expression would have an impact on the heart and that its relationship to remodeling is not simply an epiphenomenon. The direct association between galectin-3 and myocardial inflammation, dysfunction, and adverse cardiovascular outcomes post-MI was examined using clinical and translational studies. Methods: We performed expression analysis of 9753 genes in murine model of acute MI. For galectin-3 loss of function studies, homozygous galectin-3 knock-out (KO) mice were subjected to coronary artery ligation procedure to induce acute MI (MI, N = 6; Sham, N = 6). For clinical validation, serum galectin-3 levels were measured in 96 patients with ST-elevation MI. Echocardiographic and angiographic parameters of myocardial dysfunction and 3-month composite outcome including mortality, recurrent MI, stroke, and heart failure hospitalization were measured. Results: In the infarct regions of murine models, galectin-3 was a robustly expressed gene. Elevated galectin-3 expression strongly correlated with macrophage-mediated genes. Galectin-3 KO mice showed reduced myocardial macrophage infiltration after acute MI. Galectin-3 levels were higher in patients with early systolic dysfunction, and predicted 3-month major adverse cardiovascular events (area under the curve [AUC]: 0.917 ± 0.063; P = .001). Conclusions: Galectin-3 is directly associated with early myocardial inflammation post-MI and may represent a potential target for therapeutic inhibition. [ABSTRACT FROM AUTHOR]
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