This study aimed to determine the regulatory mechanism of miR-26b in myocardial infarction (MI)-induced cardiac remodeling through apoptosis.

Material and methods:
An MI rat model was established by left coronary artery ligation. Microarray data were analyzed to distinguish differentially expressed genes in MI. miR-26b was found to be poorly expressed, whereas ring finger protein 6 (RNF6) was highly expressed in MI. Consequently, miR-26b was identified to target RNF6 using dual-luciferase reporter assay and bioinformatics prediction. Furthermore, rats injected with a lentiviral vector expressing miR-26b mimic and/or RNF6 were used to evaluate the role of miR-26b and RNF6 in regulating cardiac function, infarct size, and cardiomyocyte apoptosis.

miR-26b overexpression improved cardiac function and increased left ventricular end-diastolic and end-systolic diameters. Meanwhile, incre­ased miR-26b expression decreased infarct size and cardiomyocyte apoptosis. Moreover, RNF6 overexpression counteracted the role of miR-26b in cardiac function. Additionally, an in vitro cell model illustrated that miR-26b upregulation could increase cell viability and reduce apoptosis, whereas RNF6 overexpression reversed its effect. We also found that the miR-26b mimic could negatively modulate RNF6 expression to inactivate the ER/Bcl-xL axis.

miR-26b plays a protective role against cardiac remodeling after MI through inactivation of the RNF6/ER/Bcl-xL axis, supporting miR-26b and RNF6 as potential therapeutic targets for MI.

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