论文部分内容阅读
瞬时受体电位通道(TRP)超家族组成超过50种阳离子通道,分布在几乎所有心血管组织中,可以整合多种物理和化学的刺激诱导Ca2+进入胞内。TRP通道家族对心脏节律的维持起着关键作用:TRPC可能通过钙池操纵Ca2+通道参与起搏调控;肥厚心肌中TRPM4表达上调,通过瞬时性内向电流(Iti)参与延迟后除极的发生;TR-PC1和TRPC6参与牵张诱发性心律失常的发生;在缺血缺氧的病理条件下,ATP/UTP的释放激活TRPC3/7引发心电异常。将来有望通过干预TRP活性来开发新一代的抗心律失常药物。
The Transient Receptor Potential Channel (TRP) superfamily comprises more than 50 cation channels distributed in almost all cardiovascular tissues and integrates various physical and chemical stimuli to induce Ca2 + entry into the cell. The TRP channel family plays a key role in the maintenance of cardiac rhythm: TRPC may participate in pacing regulation by Ca2 + manipulation of Ca2 + channels; upregulation of TRPM4 in hypertrophic myocardium and participation in delayed depolarization via transient inward current (Iti); TR -PC1 and TRPC6 participate in the development of stretch inducing arrhythmia; TRPC3 / 7 release of ATP / UTP triggers electrocardiographic abnormalities under hypoxic-ischemic pathology. In the future it is expected to develop a new generation of anti-arrhythmic drugs by interfering with the activity of TRP.