Background Small noncoding microRNAs regulate gene expression in cardiac development and disease and have been implicated in the aging process and in the regulation of extracellular matrix proteins. However, their rol...Background Small noncoding microRNAs regulate gene expression in cardiac development and disease and have been implicated in the aging process and in the regulation of extracellular matrix proteins. However, their role in age-related cardiac remodeling and atrial fibrillation （AF） was not well understood. The present study was designed to decipher molecular mechanisms underlying age-related atrial structural remodeling and AF. Methods Three groups of dogs were studied： adult and aged dogs in sinus rhythm and with persistent AF induced by rapid atrial pacing. The expressions of microRNAs were measured by quantitative real-time polymerase chain reaction. Pathohistological and ultrastructural changes were tested by light and electron microscopy. Apoptosis index of myocytes was detected by TUNEL. Results Samples of atrial tissue showed the abnormal pathohistological and ultrastructural changes, the accelerated fibrosis, and apoptosis with aging and/or in AF dogs. Compared to the adult group, the expressions of microRNAs-21 and -29 were significantly increased, whereas the expressions of microRNAs-1 and -133 showed obvious downregulation tendency in the aged group. Compared to the aged group, the expressions of microRNAs-1, -21, and -29 was significantly increased in the old group in AF; contrastingly, the expressions of microRNA-133 showed obvious downregulation tendency. Conclusion These multiple aberrantly expressed microRNAs may be responsible for modulating the transition from adaptation to pathological atrial remodeling with aging and/or in AE展开更多
Electrical remodeling in atrial fibrillation(AF)is considered to beget AF.However,in AF,decreased expressions of introverted ion currents INa and ICa channel proteins are corresponding to the induced increase of ion c...Electrical remodeling in atrial fibrillation(AF)is considered to beget AF.However,in AF,decreased expressions of introverted ion currents INa and ICa channel proteins are corresponding to the induced increase of ion concentration in cells to maintain the membranes’polarity;ITo is phase 1 instantaneous extraverted K+current,IKur is the important extraverted K+current in phases 1 and 2,IKr,IKs are the main extraverted current in phase 2,and the ion channel proteins of them are down-regulated in AF to prolong atrial effective refractory period(AERP),which is disadvantageous to reentry;IK1,IKAch,IKATP work in phase 3,and their up-regulated channel proteins amplify myocardium diastolic potential,lower the myocardium excitability and reduce the ectopic excitement.Therefore,in AF,atrial electrical remodeling is not to beget AF,but to restore its physiological function.AF begets AF in that it can cause atrial structural remodeling,and the structural remodeling facilitates AF initiation and perpetuation.The interaction eventually aggravates atrial muscle injury and induces myocardial electrical disorder.展开更多
Atrial fibrillation （AF） is one of the most common .arrhythmias in clinical practice. AF results in electrophysiological alterations which involve increased atrial effective refractory period and atrial effective re...Atrial fibrillation （AF） is one of the most common .arrhythmias in clinical practice. AF results in electrophysiological alterations which involve increased atrial effective refractory period and atrial effective refractory period dispersion, reduced rate adaptation of atrial effective refractory period, and slowed atrial conduction. These variances promote their own maintenance-AF begets AF.1 Previous study suggested that Ca^2＋ overload and metabolic derangement contributed to electrophysiological remodeling in AF. However, we did not demonstrate a persistent disturbance in energy metabolism during AF in our previous study,展开更多
基金This study was supported by grants from the Program of National Natural Science Foundation of China （No. 308（~60299~, tlae Program of Natural Science Foundation of the Xiniiang Uygur Autonomous Region （No. 200821143 and No. 201121 IA074）, and the Program of Doctoral Fund of Ministry of Education （No. 200807600004）.
文摘Background Small noncoding microRNAs regulate gene expression in cardiac development and disease and have been implicated in the aging process and in the regulation of extracellular matrix proteins. However, their role in age-related cardiac remodeling and atrial fibrillation （AF） was not well understood. The present study was designed to decipher molecular mechanisms underlying age-related atrial structural remodeling and AF. Methods Three groups of dogs were studied： adult and aged dogs in sinus rhythm and with persistent AF induced by rapid atrial pacing. The expressions of microRNAs were measured by quantitative real-time polymerase chain reaction. Pathohistological and ultrastructural changes were tested by light and electron microscopy. Apoptosis index of myocytes was detected by TUNEL. Results Samples of atrial tissue showed the abnormal pathohistological and ultrastructural changes, the accelerated fibrosis, and apoptosis with aging and/or in AF dogs. Compared to the adult group, the expressions of microRNAs-21 and -29 were significantly increased, whereas the expressions of microRNAs-1 and -133 showed obvious downregulation tendency in the aged group. Compared to the aged group, the expressions of microRNAs-1, -21, and -29 was significantly increased in the old group in AF; contrastingly, the expressions of microRNA-133 showed obvious downregulation tendency. Conclusion These multiple aberrantly expressed microRNAs may be responsible for modulating the transition from adaptation to pathological atrial remodeling with aging and/or in AE
文摘Electrical remodeling in atrial fibrillation(AF)is considered to beget AF.However,in AF,decreased expressions of introverted ion currents INa and ICa channel proteins are corresponding to the induced increase of ion concentration in cells to maintain the membranes’polarity;ITo is phase 1 instantaneous extraverted K+current,IKur is the important extraverted K+current in phases 1 and 2,IKr,IKs are the main extraverted current in phase 2,and the ion channel proteins of them are down-regulated in AF to prolong atrial effective refractory period(AERP),which is disadvantageous to reentry;IK1,IKAch,IKATP work in phase 3,and their up-regulated channel proteins amplify myocardium diastolic potential,lower the myocardium excitability and reduce the ectopic excitement.Therefore,in AF,atrial electrical remodeling is not to beget AF,but to restore its physiological function.AF begets AF in that it can cause atrial structural remodeling,and the structural remodeling facilitates AF initiation and perpetuation.The interaction eventually aggravates atrial muscle injury and induces myocardial electrical disorder.
文摘Atrial fibrillation （AF） is one of the most common .arrhythmias in clinical practice. AF results in electrophysiological alterations which involve increased atrial effective refractory period and atrial effective refractory period dispersion, reduced rate adaptation of atrial effective refractory period, and slowed atrial conduction. These variances promote their own maintenance-AF begets AF.1 Previous study suggested that Ca^2＋ overload and metabolic derangement contributed to electrophysiological remodeling in AF. However, we did not demonstrate a persistent disturbance in energy metabolism during AF in our previous study,
