Cardiovascular diseases (CVDs) are currently the most common cause of morbidity and mortality worldwide. Experimental studies suggest that liver kinase B1 (LKB1) plays an important role in the heart. Several studies have shown that cardiomyocyte-specific LKB1 deletion leads to hypertrophic cardiomyopathy, left ventricular contractile dysfunction, and an increased risk of atrial fibrillation. In addition, the cardioprotective effects of several medicines and natural compounds, including metformin, empagliflozin, bexarotene, and resveratrol, have been reported to be associated with LKB1 activity. LKB1 limits the size of the damaged myocardial area by modifying cellular metabolism, enhancing the antioxidant system, suppressing hypertrophic signals, and inducing mild autophagy, which are all primarily mediated by the AMP-activated protein kinase (AMPK) energy sensor. LKB1 also improves myocardial efficiency by modulating the function of contractile proteins, regulating the expression of electrical channels, and increasing vascular dilatation. Considering these properties, stimulation of LKB1 signaling offers a promising approach in the prevention and treatment of heart diseases.
Keywords: AMPK; Cardiac remodeling; Cardiovascular diseases; Cellular metabolism; LKB1.
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