一項(xiàng)小鼠研究為下述問(wèn)題提供了一個(gè)可能的解釋?zhuān)簽槭裁慈巳狈π募〖〖}蛋白心跳不規(guī)則，為什么只會(huì)在運(yùn)動(dòng)而不是其他時(shí)候發(fā)生死亡。

擬正交感神經(jīng)素多態(tài)心室心動(dòng)過(guò)速(CPVT)是一種危及生命的疾病，其特征是在運(yùn)動(dòng)時(shí)不規(guī)則心跳。CPVT可能是由編碼CASQ2的基因發(fā)生突變引起的，這是一種Ca2+結(jié)合蛋白，在心臟肌細(xì)胞中儲(chǔ)存Ca2+。盡管CASQ2被認(rèn)為在調(diào)節(jié)心臟收縮方面具有重要作用，而缺乏CASQ2以及心臟收縮相對(duì)正常的人都已經(jīng)被鑒別出來(lái)。
 
Exercise May Be Deadly for Arrhythmia Patients
 
A new study in mice has provided a potential explanation for why the heartbeat of humans lacking the protein cardiac calsequestrin (CASQ2) is irregular and potentially fatal only during exercise and not at other times.

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a life-threatening disease characterized by an irregular heartbeat during exercise. CPVT can be caused by mutations in the gene encoding CASQ2, a Ca2+ binding protein found in the Ca2+ storage facility of the muscle cells of the heart. Paradoxically, although CASQ2 is thought to have a crucial role in regulating contraction of the heart, individuals lacking both copies of CASQ2 and whose hearts contract relatively normally have been identified.