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Sci Trans Med:科学家发现抑癌小分子竟能扭转心衰!

2017-05-28 朱爽爽 奇点网

在许多国家,心血管疾病已经成为死亡率最高的“第一大杀手”了,而心血管疾病“走入末路”时导致的就是心力衰竭,尽管一些治疗心衰的药物已经被广泛使用,但是心力衰竭的患者在初次诊断后5年内的死亡率仍然高达40%(1)!

在许多国家,心血管疾病已经成为死亡率最高的“第一大杀手”了,而心血管疾病“走入末路”时导致的就是心力衰竭,尽管一些治疗心衰的药物已经被广泛使用,但是心力衰竭的患者在初次诊断后5年内的死亡率仍然高达40%!

目前比较常见的心衰药物包括β肾上腺素受体阻断剂和肾素血管紧张素转化酶抑制剂等,但是它们能做的都只是缓解心脏压力过大这一症状,不能从根本上“阻挡”心力衰竭“前进的脚步”。这样的现状提醒我们,新的治疗药物的出现是必须而紧迫的。

本月,Gladstone研究所的一个研究小组发表了《科学转化医学》封面文章,他们在心力衰竭大鼠模型以及人类细胞模型中证明了一种小分子JQ1可以治疗已经发生的心力衰竭,不仅能够缓解心力衰竭的症状,还能从基因水平扭转心力衰竭的进展!



科学转化医学封面

为了更好的理解这个研究,我们首先有必要简单了解一下心力衰竭的机制。在我们平时的生活中,一些适当的运动能够增加心脏压力,而为了应对它,心肌细胞会发生形状的改变以适应压力,保护心脏,我们称为正常“心脏重塑”。

但是值得注意的是,由疾病引起的长期持续的心肌细胞形状的改变则会导致心肌肥大,炎症,心肌成纤维细胞激活以及心脏收缩功能障碍等一系列问题,这就是病理性的心脏重塑。这种病理性心脏重塑最终就会造成心力衰竭。



正常心脏(左)心力衰竭患者的心脏(右)

此外,研究人员还发现,心肌细胞形状发生改变是与一些基因的激活有关的,再进一步说,这一激活需要由一个名为BRD4(bromodomain-containing protein 4)的蛋白介导。BRD4能够与染色体上特定区域结合以促进相应基因的表达,进而介导心肌细胞形状的改变。

由此可见,BDR4恐怕是就导致心力衰竭的罪魁祸首了。然而BDR4不仅会导致心力衰竭,在过去的研究中,研究人员发现BDR4也是新兴的癌症治疗靶点,而JQ1最初也被开发用作一种靶向BDR4的癌症治疗方案,JQ1可以高度的结构特异性以及高亲和力地与BRD4的结合抑制BDR4的功能。

因为JQ1能够与BRD4高度特异性的结合抑制其功能,所以,研究人员想,那么是不是JQ1治疗心力衰竭也是可行的呢?所以他们就开始了“漫长”的研究。2013年,他们获得了一个小突破,在大鼠模型中,JQ1抑制了BDR4的活性,阻止了病理性心脏重塑的一些症状。但这只是相当于阻止了心力衰竭“即将迈出的步伐”,而实际上,由于心血管疾病的发展,大多数心力衰竭其实已经在我们不注意的时候“无声无息”地开始了。于是,研究人员想,要是能够阻止甚至扭转已经开始的心力衰竭,那就更好了!



BRD4可以和染色体结合(左)JQ1抑制这一过程(右)

所以,他们就开展了这次的新研究。首先,要证明JQ1对已经发展的心力衰竭是有效的。研究人员首先建立了心力衰竭的大鼠模型,在建立后第18天开始接受JQ1或者安慰剂治疗,治疗一共进行8周。结果发现与安慰剂相比,JQ1明显减少了心衰小鼠心肌细胞和心脏的肥大,改善了左心室收缩功能障碍以及左心室纤维化等心力衰竭的标志性症状。

接下来,根据临床上的“经验”,研究人员总结出,由心肌梗死(MI)发展的心力衰竭是患者中最常见的一类。于是,他们又建立了心肌梗死的大鼠模型,这些大鼠中35%在手术后5天内死亡。在排除了这些没能“挺过”急性心肌梗死发作的大鼠后,剩余的大鼠在第6天接受了JQ1和安慰剂治疗,研究人员欣喜地观察到,JQ1同样显着减少了心力衰竭标志性症状的发生。这些结果表明JQ1对不同原因引起的心力衰竭是有效的。



MI大鼠接受安慰剂后(右上)心肌细胞变大而接受JQ1后(右下)与正常心肌细胞(左上)无显着差异

那么JQ1具体是如何发挥作用的呢?之前的研究已经发现了BRD4会调节基因的表达,而JQ1会抑制BDR4的功能。因此,研究人员分析对比了健康的和接受安慰剂以及JQ1治疗的心力衰竭的大鼠模型中基因表达的情况。他们发现,在前面构建的两种心力衰竭大鼠模型中,有两个不同的信号通路被抑制,一个是转化生长因子-β(TGF-β)信号通路,它本身是重要的细胞形态调节通路。另一个是与先天免疫以及炎症反应相关的NFκB信号通路。这就揭开了JQ1治疗心力衰竭的分子机制。

虽然JQ1抑制了心肌细胞的异常生长,但同样是“生长”,正常的心肌细胞生长会不会也被抑制呢?这也是很重要的,毕竟正常情况下的心肌生长对心脏保护是有利的。为了解决这个疑问,研究人员选择了健康的成年大鼠,让它们进行高强度的耐力游泳训练,每天锻炼3小时,坚持4周,再与“久卧不运动”的大鼠同时给予JQ1和安慰剂。结果显示,JQ1组和安慰剂组大鼠的心脏重量、心肌细胞横切面面积和左心室射血分数(代表心脏的收缩能力)都有了一定增加,且增加相似。这说明JQ1不会抑制正常的心脏生长。

然而,由于之前对JQ1的研究都是在大鼠模型中完成的。研究人员还想继续探索JQ1对人的心肌细胞的作用究竟如何。为此他们从志愿者身上获得了诱导性多能干细胞,再分化成心肌细胞进行培养,并使用内皮素-1(ET-1)刺激心肌细胞产生肥大症状。和大鼠同样的,JQ1减弱了心肌细胞的肥厚性增长。并且RNA测序分析显示,响应JQ1治疗的通路也是TGF-β和NFκB。这就表明了JQ1对人的心肌细胞肥大也有治疗效果。



ET-1刺激后心肌细胞变大(中),而ET-1刺激后使用JQ1(右)则与正常心肌细胞(左)无明显差异

总的来说,JQ1对于心力衰竭的治疗不同于目前的常规治疗,JQ1是作用于基因水平,可以说是从根本上抑制,甚至是扭转了心力衰竭相关症状,比如心肌肥厚的发生,这是目前心力衰竭常规治疗无法达到的。并且JQ1的安全性也在过去的癌症研究中有了一些证明,这也意味着JQ1在未来不需要太久的时间内作为新的心力衰竭治疗药物出现是很有希望的,这无疑会为心力衰竭患者带来新的希望。

原始出处:

Duan Q, McMahon S, Anand P, Shah H, Thomas S, et al. 2017. BET bromodomain inhibition suppresses innate inflammatory and profibrotic transcriptional networks in heart failure. Science Translational Medicine .

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    2017-08-06 宋威
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    2018-02-19 bsmagic9140
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    2017-05-30 1e10c84am36(暂无匿称)

    文章不错,拜读了

    0

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    2017-05-29 ylzr123

    好文,值得点赞!认真学习了,把经验应用于实践,为患者解除病痛。

    0

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    2017-05-29 lou.minghong

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