Lactate, which is an end product of glycolysis, has traditionally been considered as a metabolic waste. However, numerous studies have demonstrated that lactate serves metabolic and nonmetabolic functions in physiological processes and multiple diseases. Cancer and pulmonary arterial hypertension have been shown to undergo metabolic reprogramming, which is accompanied by increased lactate production. Metabolic reprogramming and epigenetic modifications have been extensively linked; furthermore, posttranslational modifications of histones caused by metabolites play a vital role in epigenetic alterations. In this paper, we reviewed recent research on lactate-induced histone modifications and provided a new vision about the metabolic effect of glycolysis. Based on our review, the crosstalk between the metabolome and epigenome induced by glycolysis may indicate novel epigenetic regulatory and therapeutic opportunities. There is a magnificent progress of the interaction between metabolomics and epigenomics in recent decades, but many questions still remained to be investigated. Lactylation is found in different pathophysiological states and leads to diverse biological effects, however, only a few mechanisms of lactylation have been illustrated. Further research on lactylation would provide us with a better understanding of the crosstalk between the metabolomics and epigenomics.
Multifocal atrial tachycardia (MAT) is defined as irregular P-P, R-R, and P-R intervals, isoelectric baseline between P waves, and ventricular rate over 100 beats/min. Although the prognosis of pediatric MAT in most patients is favorable, adverse outcomes of MAT have been reported, such as cardiogenic death (3%), respiratory failure (6%), or persistent arrhythmia (7%), due to delayed diagnosis and poorly controlled MAT. Previous studies demonstrated that pediatric MAT is associated with multiple enhanced automatic lesions located in the atrium or abnormal automaticity of a single lesion located in the pulmonary veins via multiple pathways to trigger electrical activity. Recent studies indicated that pediatric MAT is associated with the formation of a re-entry loop, abnormal automaticity, and triggering activity. The occurrence of pediatric MAT is affected by gestational disease, congenital heart disease, post-cardiac surgery, pulmonary hypertension, and infectious diseases, which promote MAT via inflammation, redistribution of the autonomic nervous system, and abnormal ion channels. However, the pathogenesis of MAT needs to be explored. This review is aimed to summarize and analyze the pathogenesis in pediatric MAT.
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