心房颤动与miRNA

Atrial fibrillation and miRNA

  • 摘要: 心房颤动(房颤)的发生、发展机制复杂,除心脏解剖结构外,心脏结构重构、电重构、自主神经系统调节以及钙离子(Ca2+)运转异常均可引起局灶异位放电而引发房颤,或通过一个折返机制触发折返性房颤发生并持续也是导致房颤的重要机制。深入研究发现微RNA(miR)调控信使RNA可以改变有关路径、离子通道蛋白、转运蛋白等的合成和降解,进而影响离子流导致Ca2+运转异常、心脏电重构;影响成纤维细胞导致组织纤维化,引起心脏结构性重构,最终引发房颤。心脏的发育、细胞增殖、引起房颤的折返机制的基质形成等都与miR相关,miR有望成为诊断房颤新的生物标志物和上游治疗的新靶点。

     

    Abstract: The mechanism underlying atrial fibrillation (AF) is not completely understood due to its complexity. In addition to anatomical structure of the heart, structural remodeling, electrical remodeling, autonomic nervous system regulation, and calcium ion (Ca2+) malfunctioning can also cause focal ectopic discharges and trigger AF. Moreover, triggering the incidence and persistence of reentrant AF through a reentry maintenance mechanism is also an important mechanism leading to AF. Further studies have found that the synthesis and degradation of related pathways, ion channel proteins and transporters can be changed through the role of microRNA (miR) inregulating messenger RNA. It not only affects the ionic current, leading to abnormal Ca2+ transport and cardiac electrical remodeling,but also influences fibroblasts, resulting in tissue fibrosis andstructural remodeling, and eventually inducing the incidence and maintenance of AF. Cardiac development, cardiomyocyte proliferation and substrate formation due to reentry mechanism causing AF were correlated with miR. MiR would become a novel biomarker for diagnosis of AF and a novel target for upstream treatment.

     

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