The role of Asprosin in patients with dilated cardiomyopathy
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RESEARCH ARTICLE
Open Access
The role of Asprosin in patients with dilated cardiomyopathy Ming-Shien Wen1*, Chao-Yung Wang1,2* , Jih-Kai Yeh1, Chun-Chi Chen1, Ming-Lung Tsai1, Ming-Yun Ho1, Kuo-Chun Hung1 and I-Chang Hsieh1
Abstract Background: Asprosin is a novel fasting glucogenic adipokine discovered in 2016. Asprosin induces rapid glucose releases from the liver. However, its molecular mechanisms and function are still unclear. Adaptation of energy substrates from fatty acid to glucose is recently considered a novel therapeutic target in heart failure treatment. We hypothesized that the asprosin is able to modulate cardiac mitochondrial functions and has important prognostic implications in dilated cardiomyopathy (DCM) patients. Methods: We prospectively enrolled 50 patients (86% male, mean age 55 ± 13 years) with DCM and followed their 5-year major adverse cardiovascular events from 2012 to 2017. Comparing with healthy individuals, DCM patients had higher asprosin levels (191.2 versus 79.7 ng/mL, P < 0.01). Results: During the 5-year follow-up in the study cohort, 16 (32.0%) patients experienced adverse cardiovascular events. Patients with lower asprosin levels (< 210 ng/mL) were associated with increased risks of adverse clinical outcomes with a hazard ratio of 7.94 (95% CI 1.88–33.50, P = 0.005) when compared patients with higher asprosin levels (≥ 210 ng/mL). Using cardiomyoblasts as a cellular model, we showed that asprosin prevented hypoxiainduced cell death and enhanced mitochondrial respiration and proton leak under hypoxia. Conclusions: In patients with DCM, elevated plasma asprosin levels are associated with less adverse cardiovascular events in five years. The underlying protective mechanisms of asprosin may be linked to its functions relating to enhanced mitochondrial respiration under hypoxia. Keywords: Asprosin, Dilated cardiomyopathy, Heart failure, Hypoxia, Obesity
Introduction Heart failure (HF) is a growing global public health problem, particularly in the elderly population, affecting more than 26 million patients worldwide [1]. The health care expenditure attributed to heart failure in Europe and North America reaches around 1–2% recently [2, 3]. Despite encouraging advances in heart failure medications and device therapy, mortality and readmission rates in HF patients are still around 15–30% over the past 15 * Correspondence: [email protected]; [email protected] 1 Department of Cardiology, Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, 5 Fu-Hsing Street, Taoyuan 333, Taiwan Full list of author information is available at the end of the article
years [4]. The development of new therapeutics to avoid HF readmission are the current major target of many studies. Therefore, it is imperative to explore a novel mechanism to prevent heart failure or to develop an efficient target for improving heart function [5]. Most current HF treatments emphasize reducing myocardial workload and energy consumption, such as alleviating preload or afterload, reducing heart rate, an
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