RESUMO
Atrial fibrillation (AF) is a common cardiac arrhythmia that often occurs in patients with structural heart disease and is a significant cause of morbidity and mortality in clinical settings. AF is typically associated with significant changes of both the structure of the atria and the cardiac conduction system. AF can result in reduced heart function, heart failure, and various other complications. Current drug therapy for AF patients is often ineffective and may have adverse effects. Radiofrequency ablation is more effective than traditional drug therapy, but this invasive procedure carries potential risks and may lead to postoperative recurrence, limiting the clinical benefits to some extent. Therefore, in-depth research into the molecular mechanisms of AF and exploration of new treatment strategies based on research findings are prerequisites for improving the treatment of AF and the associated cardiac conditions. Long noncoding RNAs (lncRNAs) are a new class of noncoding RNA (ncRNAs) with a length exceeding 200 nt, which regulate gene expression at multiple levels. Increasing evidence suggests that lncRNAs participate in many pathological processes of AF initiation, development, and maintenance, such as structural remodeling, electrical remodeling, renin-angiotensin system anomalies, and intracellular calcium deregulation s. LncRNAs that play key roles in structural and electrical remodeling may become molecular markers and targets for AF diagnosis and treatment, respectively, while lncRNAs critical to autonomic nervous system remodeling may bring new insights into the prognosis and recurrence of AF. This review article provides a synopsis on the up-to-date research findings relevant to the roles of lncRNAs in AF.
RESUMO
Atrial fibrillation (AF), a common arrhythmia that usually occurs in patients with heart disease, is one of the leading causes for mortality and disability worldwide. Current drug therapy for AF patients lacks sufficient efficacy and has side effects. Radiofrequency ablation is more effective than traditional drug therapy, but this invasive procedure is associated with potential risks and postoperative recurrence, limiting the clinical benefits for AF patients. Therefore, it is necessary to expand our understanding about the underlying molecular mechanism of AF and to explore the new therapeutic strategies. Long noncoding RNA (lncRNA) is a set of noncoding RNA longer than 200 nucleotides. Growing evidence indicates that lncRNA is involved in numerous pathophysiological processes of AF, such as structural remodeling, electrical remodeling, renin-angiotensin system, abnormal calcium regulation, etc. In addition, lncRNA involved in structural remodeling and electrical remodeling has the potential to be a novel target for the diagnosis and treatment of AF, and lncRNA involved in autonomic nerve remodeling may bring new enlightenment for the prognosis and recurrence of AF.
Assuntos
Fibrilação Atrial , Remodelamento Atrial , RNA Longo não Codificante , Fibrilação Atrial/genética , Humanos , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Recidiva , Sistema Renina-AngiotensinaRESUMO
Objective: To observe the impact of high thoracic epidural blockade (HTEB) on atrial autonomic nerve remodeling in dogs with atrial ifbrillation (AF) induced by long-term rapid right atrial appendage pacing and to explore the effect of nerve growth factor (NGF) on atrial autonomic nerve remodeling. Methods: AF model was established by consistent rapid atrial pacing for 6 weeks. 18 experimental dogs were randomly divided into 3 groups: Sham group, the dogs had no pacing while received normal saline injection; Control group, the dogs had pacing and normal saline injection; HTEB group, the dogs had pacing and 0.5% lidocaine injection for HTEB.n=6 in each group. Atrial myocardium collagen volume fraction (CVF) was examined by Masson staining; sprouting of NGF related protein 43 (GAP43) and tyrosine hydroxylase (TH) were assessed by immunohistochemistry; protein expressions of NGF, GAP43 and TH were measured by Western blot analysis. Results: Compared with Sham group, HTEB group showed decreased CVF and sprouting of GAP43, TH,P Conclusion: Long-term rapid atrial pacing induced AF dog had inhomogeneous sprouting of atrial myocardial nerve which may cause autonomic nerve remodeling; NGF played the important role in such process. HTEB could effectively inhibit NGF up-regulation and suppress the autonomic nerve remodeling in experimental dogs.
RESUMO
Aim To investigate the preventive effect of Guizhi decoction on cardiac sympathetic sprouting induced by 4-Methylcatechol (4-MC) . Methods The rat models of cardiac sympathetic sprouting were in-duced by 10 mg · L-1 4-MC ( 10μg · kg-1 body weight, i. p. ) . Guizhi decoctions ( with different pro-portion between Ramulus Cinnamomi and Radix Paeon-iae Alba, 1 : 1, 1 : 2 and 2 : 1) and metoprolol were administered to the rats. Heart rate and electrocardio-gram ( ECG ) were observed, the content of norepi-nephrine (NE), growth associated protein (GAP-43), tyrosine hydroxylase ( TH ) and acetylcholine transfer-ase enzyme ( CHAT) in myocardial homogenate of left ventricular and right atrial were determined by ELISA method, and immunofluorescence assay was used to observe cardiac nerve sprouting and sympathetic distri-bution. Results 4-MC caused cardiac sympathetic sprouting and parasympathetic was not influenced. Heart rate of the model group was improved significant-ly and higher than that of the other groups . Compared with the model group, the content of NE, GAP-43 and TH in left ventricle and right atrium of the metoprolol group and Guizhi decoction group were decreased( P<0.05 ) , and the immunofluorescence result showed that the distribution of TH positive nerve was reduced sig-nificantly(P<0.05). It was demonstrated that Guizhi decoction of the proportion between Ramulus Cinnamo-mi and Radix Paeoniae Alba 1 : 1 and 1 : 2 had the best efficacy, which was similar to the efficacy of meto-prolol. Conclusion Guizhi decoction ( with the pro-portion between Ramulus Cinnamomi and Radix Paeon-iae Alba 1 : 1 and 1 : 2 ) effectively inhibits the cardi-ac sympathetic sprouting induced by 4-MC.
