Abstract
BackgroundAsprosin 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.MethodsWe 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).ResultsDuring 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 hypoxia-induced cell death and enhanced mitochondrial respiration and proton leak under hypoxia.ConclusionsIn 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.
Highlights
Heart failure (HF) is a growing global public health problem, in the elderly population, affecting more than 26 million patients worldwide [1]
Our results demonstrated that asprosin, a novel glucogenic protein adipokine, exerts cardiac protective effects in patients with dilated cardiomyopathy (DCM)
The OLFR734 is most abundant in the olfactory epithelium and adipose tissues [25]. It remained to be determined whether OLFR734 is the asprosin receptor in the cardiomyocytes and future study will be needed to investigate the signaling pathway of which asprosin exerts its protection from hypoxia in the heart and DCM patients
Summary
Heart failure (HF) is a growing global public health problem, 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]. Most current HF treatments emphasize reducing myocardial workload and energy consumption, such as alleviating preload or afterload, reducing heart rate, and modulating neurohormonal activation [6]. Studies have focused on cardiac energy metabolism. This leads to the discovery of several novel compounds to balance the energy expenditure mismatching of HF patients [7, 8]. 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
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