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Nicotinamide Phosphoribosyltransferase (Nampt)/Nicotinamide Adenine Dinucleotide (NAD)Axis Suppresses Atrial Fibrillation by Modulating the Calcium Handling Pathway

馮, 鐸 筑波大学 DOI:10.15068/0002001926

2021.11.24

概要

Atrial fibrillation (AF) has received widespread attention from both clinicians and scientists for over a century. It is the most common arrhythmia encountered in clinical practice and is characterized by irregular atrial electrical activity resulting in asynchronous atrial contraction. AF increases the risk of embolic stroke, heart failure, and overall mortality [1–3], and is global problem affecting more than 33 million people worldwide [4]. Current therapeutic options have limited efficacy and substantial adverse effects, and there is a clear need for further therapeutic innovation. All forms of AF arise from interactions between genetic predisposition, advancing age, environmental factors, and cardiovascular/non-cardiovascular disease, which disturb normal atrial electrophysiology, promoting focal ectopic activity and re- entry, the fundamental arrhythmogenic mechanisms underlying AF initiation and maintenance. Of note, these components are also strongly modulated by AF itself. All the risk factors and co-morbidities are modulated by numerous mediators such as oxidative stress, autonomic imbalance, calcium handling abnormalities, altered atrial metabolism, pulmonary vein, structural remodeling and electrical remodeling. Previous studies showed that aging and obesity are two of the most prominent risk factors for AF occurrence [5– 7]. In obesity, cardiometabolic changes in the heart favor reactive oxygen species (ROS) production [8,9]. Oxidative stress activates calmodulin-dependent protein kinase II (CaMKII), leading to arrhythmogenic hyperphosphorylation of RyR2. Oxidized CaMKII-mediated hyperphosphorylation of RyR2 promotes diastolic calcium leaks from the sarcoplasmic reticulum (SR) in atrial cardiomyocytes, causing AF [10,11]. Therefore, oxidized CaMKII and its downstream components may be promising therapeutic targets for prevention of AF.

　Nicotinamide phosphoribosyltransferase (Nampt), also known as pre-B cell colony-enhancing factor (PBEF) or visfatin, represents a 52 kDa pleiotropic molecule, encoded by NAMPT gene, acting as an enzyme, a cytokine/adipocytokine, and a growth factor. It plays an important role in cellular bioenergetics and metabolism, particularly nicotinamide adenine dinucleotide (NAD) biosynthesis [12]. NAD and its phosphorylated form NADP are indispensable coenzymes acting as electron carriers in cellular energetics and counteraction of intracellular oxidative stress. NAD cellular metabolism, via NAD-consuming enzymes as regulators of NAD+/NADH bioavailability, is critical in DNA repair, genomic integrity, oncogenic signal transduction and transcription, apoptosis and is a substrate for NAD-dependent enzymes like sirtuin 1 (Sirt1) [13]. The Nampt/NAD/Sirt1 axis has protective roles against aging and obesity-related disorders such as type 2 diabetes mellitus by influencing the oxidative stress response, apoptosis, lipid and glucose metabolism, inflammation, and insulin resistance [14–18]. Nampt is highly expressed in cardiomyocytes, and recent studies have demonstrated its effects on a variety of cardiac morbidities, including dilated cardiomyopathy, ischemia/reperfusion injury, and heart failure [19–21]. However, there have been no reports on the relationship between AF and Nampt. Because the Nampt/NAD axis is involved in obesity and aging, the most important risk factors for AF, we hypothesized that the Nampt/NAD axis has an important role in the pathogenesis of obesity-induced AF. To achieve that, we used heterozygous Nampt knockout mice (NKO), wild-type (WT) littermate mice as control and tried to clarify whether Nampt is involved in an 8 weeks high-fat- diet (HFD)-induced atrial arrhythmogenic remodeling mice.

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