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Article(id=1241311711790158609, tenantId=1146029695717560320, journalId=1205117082300743687, issueId=1241311708883513558, articleNumber=null, orderNo=null, doi=10.14109/j.cnki.xyylc.2024.01.04, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1650988800000, receivedDateStr=2022-04-27, revisedDate=null, revisedDateStr=null, acceptedDate=1683043200000, acceptedDateStr=2023-05-03, onlineDate=1773881374547, onlineDateStr=2026-03-19, pubDate=1706112000000, pubDateStr=2024-01-25, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1773881374547, onlineIssueDateStr=2026-03-19, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1773881374547, creator=13701087609, updateTime=1773881374547, updator=13701087609, issue=Issue{id=1241311708883513558, tenantId=1146029695717560320, journalId=1205117082300743687, year='2024', volume='43', issue='1', pageStart='1', pageEnd='78', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1773881373854, creator=13701087609, updateTime=1773882024061, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1241314436116435425, tenantId=1146029695717560320, journalId=1205117082300743687, issueId=1241311708883513558, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1241314436116435426, tenantId=1146029695717560320, journalId=1205117082300743687, issueId=1241311708883513558, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=17, endPage=21, ext={EN=ArticleExt(id=1241311713530794771, articleId=1241311711790158609, tenantId=1146029695717560320, journalId=1205117082300743687, language=EN, title=Research progress of miR-132 and its inhibitors in heart failure, columnId=1207314219599499390, journalTitle=Chinese Journal of New Drugs and Clinical Remedies, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

miR-132 is a widely expressed regulatory RNA in the cardiovascular system. When miR-132 is highly expressed in cardiac tissues, it will affect the signaling pathways related to cardiomyocyte growth, autophagy, calcium processing and contraction, and cause progressive adverse cardiac remodeling, thus leading to heart failure events. Studies had found that targeted inhibition of miR-132 could reduce cardiac hypertrophy and improve cardiac function, bringing certain clinical benefits to patients with heart failure. CDR132L is a synthetic lead-optimized oligonucleotide inhibitor of miR-132.The efficacy and safety of CDR132L had been demonstrated for the first time in clinical trials. Antisense oligonucleotides targeting miR-132 are potential future therapies for ischemic or non-ischemic heart failure.

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miR-132是一种在心血管系统中普遍表达的调节RNA。当心脏组织中的miR-132高表达时，会影响与心肌细胞生长、自噬、钙处理和收缩等相关的信号通路，引起进行性不良心脏重构，从而导致心力衰竭事件。研究发现对miR-132的靶向抑制可减轻心脏肥大并改善心脏功能，给心衰患者带来一定的临床获益。一种优化的miR-132反义寡核苷酸抑制剂CDR132L的疗效及安全性首次在临床试验中得到证明。针对miR-132的反义寡核苷酸是未来缺血性或非缺血性心力衰竭的潜在治疗方法。

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刘永铭，E-mail：
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王华，女，硕士在读，主要从事老年心血管病的研究，E-mail：

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王华，女，硕士在读，主要从事老年心血管病的研究，E-mail：

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王华，女，硕士在读，主要从事老年心血管病的研究，E-mail：

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miR-132及其抑制剂在心力衰竭中的研究进展
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王华 1 , 贾晓艳 1 , 刘永铭 2
中国新药与临床杂志 | 综述 2024,43(1): 17-21
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中国新药与临床杂志 | 综述 2024, 43(1): 17-21
miR-132及其抑制剂在心力衰竭中的研究进展
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王华1 , 贾晓艳1, 刘永铭2
作者信息
  • 1.兰州大学第一临床医学院，甘肃 兰州　730000
  • 2.兰州大学第一医院 老年心血管科，甘肃 兰州　730000

    • 王华，女，硕士在读，主要从事老年心血管病的研究，E-mail：

通讯作者:

刘永铭，E-mail：
Research progress of miR-132 and its inhibitors in heart failure
Hua WANG1 , Xiao-yan JIA1, Yong-ming LIU2
Affiliations
  • 1.The First Clinical Medical College of Lanzhou University, Lanzhou GANSU 730000, China
  • 2.Department of Geriatric Cardiology, the First Hospital of Lanzhou University, Lanzhou GANSU 730000, China
出版时间: 2024-01-25 doi: 10.14109/j.cnki.xyylc.2024.01.04
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摘要
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miR-132是一种在心血管系统中普遍表达的调节RNA。当心脏组织中的miR-132高表达时，会影响与心肌细胞生长、自噬、钙处理和收缩等相关的信号通路，引起进行性不良心脏重构，从而导致心力衰竭事件。研究发现对miR-132的靶向抑制可减轻心脏肥大并改善心脏功能，给心衰患者带来一定的临床获益。一种优化的miR-132反义寡核苷酸抑制剂CDR132L的疗效及安全性首次在临床试验中得到证明。针对miR-132的反义寡核苷酸是未来缺血性或非缺血性心力衰竭的潜在治疗方法。

微RNAs  /  miR-132  /  心力衰竭  /  心脏扩大  /  CDR132L

miR-132 is a widely expressed regulatory RNA in the cardiovascular system. When miR-132 is highly expressed in cardiac tissues, it will affect the signaling pathways related to cardiomyocyte growth, autophagy, calcium processing and contraction, and cause progressive adverse cardiac remodeling, thus leading to heart failure events. Studies had found that targeted inhibition of miR-132 could reduce cardiac hypertrophy and improve cardiac function, bringing certain clinical benefits to patients with heart failure. CDR132L is a synthetic lead-optimized oligonucleotide inhibitor of miR-132.The efficacy and safety of CDR132L had been demonstrated for the first time in clinical trials. Antisense oligonucleotides targeting miR-132 are potential future therapies for ischemic or non-ischemic heart failure.

microRNAs  /  miR-132  /  heart failure  /  cardiomegaly  /  CDR132L
王华, 贾晓艳, 刘永铭. miR-132及其抑制剂在心力衰竭中的研究进展. 中国新药与临床杂志, 2024 , 43 (1) : 17 -21 . DOI: 10.14109/j.cnki.xyylc.2024.01.04
Hua WANG, Xiao-yan JIA, Yong-ming LIU. Research progress of miR-132 and its inhibitors in heart failure[J]. Chinese Journal of New Drugs and Clinical Remedies, 2024 , 43 (1) : 17 -21 . DOI: 10.14109/j.cnki.xyylc.2024.01.04
正文
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心力衰竭（心衰）是所有心血管疾病的终点，收缩功能下降导致心输出量降低和心室充盈压增加，从而导致一系列的临床症状。全球大约有2 600余万心衰患者，我国心衰患者超过1 370万（患病率1.3%），已成为65岁以上患者住院的首要原因，心衰患者出院后30 d内的再住院率为24%，约50%的心衰患者在5年内死亡[1]。心衰患者反复住院、活动耐受性差，严重影响其生活质量。近年来，心衰治疗领域相关药物研究层出不穷，但主要集中于保护心脏免受继发性神经激素过度驱动及维持心脏负荷容量等方面[2]。延缓心脏重构、恢复心脏功能是突破治疗瓶颈的关键，也是当前面临的最大困境。miR-132已被认定为影响心衰的关键分子，也是最有前景的靶点之一[3]。在慢性心衰患者中，循环miR-132水平随着心衰严重程度而上升，miR-132水平降低可减少心衰再入院的风险[4]。针对微小RNA（miRNA）的疗法一直停留在理论和实验室中，临床转化始终停滞不前。然而，最新的临床试验研究结果显示miR-132抑制剂在心衰治疗中安全且有效，可显著改善慢性心衰患者的心功能及临床预后[5]。
miR-132调节心功能的作用机制
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miRNA是一类内源性非编码RNA分子，其长度约为22 ~ 23个核苷酸，由RNase Ⅲ核酸内切酶加工产生，miRNA基因可以定位在编码基因（宿主基因）的内含子中，也可以定位在没有编码活性的区域[6]。miRNA调控许多重要的生物途径，处于基因调控网络的核心位置。近年来越来越多的研究显示，miR-132在心脏组织中上调以应对心肌细胞压力，其表达水平与心肌重构呈正相关，在心衰的发生发展中起关键作用，是心衰预后的独立危险因素[7]。
1　影响心肌电生理
心肌肌浆网Ca2+-ATP酶（SERCA2a）通过调节细胞内Ca2+浓度在调节心脏收缩和舒张方面发挥着关键作用。SERCA2a表达或活性减弱会导致钙稳态受损，引起与心衰进展相关的收缩功能障碍。研究发现miR-132是SERCA2a的调节剂[8]，在终末期心衰患者中，miR-132在心肌细胞中过度表达，通过与SERCA2a的mRNA 3'非编码区（3'UTR）结合抑制其表达，延长心肌细胞Ca2+瞬态的衰变[9]。另外，过度表达miR-132使心肌细胞中Ca2+的流入速度明显放缓，导致Ca2+瞬变达峰时程和肌节缩短时间显著延长。研究发现抑制miR-132可使不同阶段Ca2+瞬变达峰时程缩短，干预心肌细胞的收缩特性，同时恢复心脏组织中SERCA2a的表达水平[10]。LEI等[8]观察到与野生对照组相比，敲除miR-132小鼠心肌收缩力增强，且舒张期心肌肌浆网Ca2+更少，Ca2+瞬变衰减时间缩短，Ca2+的再摄取速度显著加快。
心室动作电位时程延长是心衰的标志[11]，由于钾通道下调和钙内流上调，在动作电位上表现为复极期和平台期时间延长[12]，且发生恶性室性心律失常的风险增加。研究发现抑制miR-132后，心室动作电位振幅和上升速度不受影响，但动作电位持续时间恢复为正常值，可以看出抑制miR-132的表达不会影响钠通道，主要通过影响钾通道和钙通道来恢复心室动作电位时程，从而保持心脏收缩功能和减缓心衰进展。
2　调节磷脂酰肌醇3激酶（PI3K）、蛋白激酶B（Akt）通路
磷酸酶和张力蛋白同源物（PTEN）是一种多功能脂质磷酸酶，PTEN的丢失会导致血管平滑肌细胞（VSMC）增殖、血管重塑和氧化应激，最终导致心衰[13]。研究发现PTEN是miR-132的下游目标[14]，miR-132通过直接结合到mRNA 3'UTR来介导PTEN的下调，引起PI3K/Akt信号通路的激活，PI3K/Akt信号通路通过雷帕霉素靶蛋白（mTOR）、糖原合酶激酶（GSK）-3、叉头框蛋白（Fox）O1/3和一氧化氮合酶（NOS）等转录相关基因靶点促进心肌肥大、氧化应激、心肌纤维化、自噬的发生和进展[15]。研究发现抑制miR-132的表达会使PTEN显著上调[16]，进而消极调节PI3K-Akt通路和下游目标，减轻心肌纤维化程度，改善心脏功能障碍[17]。
3　调节神经内分泌激素
甲基化CpG结合蛋白2（MeCP2）是miR-132的目标靶点，miR-132可以通过靶向MeCP2的表达促进血管加压素（AVP）合成与释放，AVP诱导水通道蛋白-2表达，并在肾脏中重新吸收水分。AVP通过水潴留、低钠血症和动脉血管收缩导致心衰发生。BIJKERK等[18]发现miR-132是第一个通过调节下丘脑AVP mRNA表达来调节渗透平衡的miRNA，进而发现抑制miR-132表达会使得水通道蛋白-2总量及血浆膜表达减少，AVP水平降低，产生急性利尿效果，改善心衰症状。miR-132也可以通过直接与血管紧张素Ⅱ（Ang Ⅱ）受体（AT1R）mRNA编码区域的序列识别位点结合来调节AT1R信号，促进心脏肥大，导致高血压及心衰的发展[19]。ESKILDSEN等[20]同样发现miR-132与Ang Ⅱ诱导的高血压有关，当miR-132被抑制后可明显改善Ang Ⅱ诱导的心肌细胞肥大以及心脏成纤维细胞的增殖和激活[21]。
4　调节沉默信息调节因子1（SIRT1）/核因子相关因子2（Nrf2）信号通路
SIRT1是依赖烟酰胺腺嘌呤二核苷酸（NAD）的脱乙酰基酶，激活SIRT1能增强线粒体的功能、促进氧化代谢。miR-132通过直接抑制SIRT1的表达[22]，使红系衍生的Nrf2生成减少。Nrf2是调控细胞氧化应激反应的重要转录因子，同时也是维持细胞内氧化还原稳态的中枢调节者，在保持心肌细胞和心肌成纤维细胞的正常功能以及防止不良的心脏重构和心衰方面发挥着重要作用[23]。研究发现通过抑制miR-132可以激活SIRT1/Nrf2信号通路，从而抑制氧化应激，减少核苷酸结合寡聚化结构域样受体蛋白（NLRP）3、caspase-1和白细胞介素（IL）-1β的基因表达，最终改善心肌缺血-再灌注损伤[22]。
5　调节Ras-有丝分裂原激活蛋白激酶（MAPK）通路
血管生成对于维持心脏组织的氧气和营养供应至关重要[24]，miR-132在体内VSMC中表达丰富，在调节血管内皮对血管生成刺激的反应方面发挥着关键作用[25]。miR-132通过靶向抑制内皮中的p120 Ras GTPase激活蛋白（Ras-GAPs）和Spred1导致Ras激活[26]，Ras蛋白是调节细胞生长和增殖信号通路的重要元件，促进下游的MAPK信号级联过度激活。Ras/MAPK通路的过度激活引起细胞的异常增殖，并且伴随着活性氧（ROS）的过度累积，促进了心肌细胞功能障碍及缺血性心衰的发展[27]。但目前关于miR-132对血管生成的影响仍然存在争议，需要在未来的研究中进一步澄清。
miR-132抑制剂相关研究
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为了评估miR-132抑制剂对心衰的疗效，FOINQUINOS等[10]设计了一种优化的合成锁定反义寡核苷酸抑制剂（antimiR-132），其主干完全磷酸化以对抗miR-132。研究发现，过度表达miR132的转基因小鼠表现出严重的左心室肥大、射血分数降低和心脏扩张，在连续使用antimiR-132（每周20 mg·kg-1）或安慰剂（生理盐水）4周后，antimiR-132组小鼠心脏组织中的功能性miR-132水平降低，显示antimiR-132可以降低心脏质量，改善射血分数并减轻心室扩张。随后研究人员进行了一项大型动物药动学研究，进一步评估antimiR-132治疗潜力，使用安慰剂和3种antimiR-132的剂量水平（1、5和10 g·kg-1）对心肌梗死（心梗）后心衰猪模型进行56 d观察，结果发现与安慰剂组相比，antimiR-132组射血分数显著增加，呈剂量依赖性。antimiR-132组心梗后左室收缩末期容积的增加被有效阻止，且随着时间的推移，这种影响更加明显。进一步分析发现，在心梗后第56日，对照组N-末端脑钠肽前体（NT-proBNP）水平显著升高，但antimiR-132显著逆转了NT-proBNP的升高。纤维化组织学评估显示，间质纤维化呈剂量依赖性降低，这表明antimiR-132组的整体心脏重构有所改善。此外，不同剂量治疗组之间的心肌疤痕组织大小没有差异。以上研究表明antimiR-132通过降低心脏质量、改善射血分数、减轻心室扩张，从而改善心肌细胞功能障碍。且在抗心脏重构的同时，不会影响心梗后心肌疤痕的演变及其周围的血管重建。这说明无论心衰患者处于何种临床阶段，均可在抗miR-132治疗中获益。
HINKEL等[28]通过在胸主动脉植入经皮还原支架，建立了一种新型的压力过载诱导心力衰竭的猪模型，分为假手术组和antimiR-132组，于制模当日和第28日将antimiR-132注入左冠状动脉（左前降支、旋支），累积剂量为0.5 mg·kg-1。在第8周时，与对照组相比，antimiR-132组心肌中抗氧化防御基因主调节剂Nrf2表达增加，表明antimiR-132治疗后心脏组织的抗氧化能力增强，激活SIRT1/Nrf2信号通路，从而抑制氧化应激和细胞凋亡，减轻心肌损伤。此外，antimiR-132组的左室舒张末压降低，左室射血分数改善［（48.9±1.0）% vs.（36.1±1.7）%］，心肌细胞横截面面积缩小［（188.9±2.8）μm2 vs.（258.4±9.0）μm2］，间质纤维化的增加幅度降低，这表明antimiR-132阻止了心肌从生理肥厚向病理肥厚的过渡。因此抑制miR-132是预防肥厚性心脏病心力衰竭进展的有效策略，可以作为非缺血性心衰的治疗方法。该研究在冠状动脉中给予2次antimiR-132来预防心肌病理肥大状态，但静脉注射更高剂量的antimiR-132能否达到类似的效果，还需要进一步研究。
近年来研发的一种优化的miR-132反义寡核苷酸抑制剂CDR132L，已经被证明可以使心肌细胞正常化，并预防和逆转心肌的病理重构过程。研究人员发现，心衰猪模型静脉注射CDR132L（5 mg·kg-1）6个月后[29]，与安慰剂相比，CDR132L组心脏组织和血液中miR-132的水平剧烈下降，左室射血分数绝对值增加了近8%。CDR132L还对左心室和左心房重构具有治疗效果，可以显著减弱心梗后左室收缩末期容积的增加，也减少了心梗后左心房体积的增加。心室和心房指数［包括左室收缩末期容积指数、左室舒张末期容积指数、左房容积指数］的降低进一步证实了这一结论。同时，治疗组NT-proBNP也明显下降，表明CDR132L治疗降低了心室壁的应力。与安慰剂相比，治疗组的间质纤维化程度明显降低，心脏梗死远端区域的平均心肌细胞体积也显著缩小，表明CDR132L减少了心肌纤维化和不良的心肌细胞肥大。进一步研究发现，CDR132L治疗的动物体内有14种mRNA的表达水平发生明显改变，其中大多数都和纤维化、心肌肥大、血管生成和血管功能有关。该研究表明CDR132L治疗可显著改善心脏功能，逆转心脏重构，突显了心衰患者的临床应用潜力。
最新的CDR132L单中心临床试验[5]是一项随机、双盲、安慰剂对照、剂量递增的临床研究，评估CDR132L对慢性缺血性心衰患者的影响。将左室射血分数30%~50%或NT-proBNP≥125 ng·L-1的28例患者随机分配至CDR132L（0.32、1、3和10 mg·kg-1）组和安慰剂（生理盐水）组，随访持续4个月。结果发现，CDR132L组患者血浆中的miR-132水平持续性地下降，其中3或10 mg·kg-1 CDR132L治疗的患者血浆miR-132水平与健康人群基本一致；NT-proBNP含量平均下降了23.3%；心肌纤维化相关的生物标志物，包括基质金属蛋白酶（MMP）-1、半乳糖凝集素（gal）-3、可溶性生长刺激表达因子-2（sST2）、中性粒细胞明胶酶相关脂质运载蛋白（NGAL）也出现了明显的降低，表明CDR132L可改善患者心功能及心肌纤维化。既往研究显示，QRS波群变窄可预测心衰患者的治疗临床获益。在对照组中，心衰患者（初始持续时间> 120 ms）的QRS波群进一步增宽，而CDR132L组患者QRS波群显著变窄（P = 0.033 3），这表明CDR132L对心衰患者的预后可能产生有益影响。这是第一项针对miR-132的人类研究，也是miRNA治疗心血管疾病领域的一个里程碑。虽然患者样本量不大，但研究结果有力地证明CDR132L可为接受标准治疗的慢性心衰患者带来一定的临床获益。但CDR132L在心衰的治疗中是否可以有效地缓解症状及体征、改善患者日常活动能力、提升患者生活质量在很大程度上仍然未知，未来有必要开展更大规模的临床研究，进一步证实CDR132L在心衰治疗领域的积极作用。
miR-132的安全性和耐受性
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临床前评估通过监测C反应蛋白、白细胞计数、肝肾损伤标记物等与安全相关的实验室参数，发现antimiR-132治疗是安全且耐受性良好，所有测量参数均在正常范围内，动物生长及IL-6和肿瘤坏死因子α（TNF-α）等炎症介质的表达并未受到antimiR-132治疗的影响[28]。CDR132L治疗同样没有观察到药物引起的不良事件或血液学和实验室指标的变化，进一步支持了之前证明的药物安全性[5]。由于某些第一代反义寡核苷酸（ASO）会出现血小板减少症[30]，研究发现当CDR132L用药剂量维持在0.32 ~ 10 mg·kg-1范围内，血小板计数在整个过程中保持正常和稳定，未见可见的肝肾毒性和血液系统毒性；高敏肌钙蛋白T和QT间期的监测结果证实，CDR132L没有明显的心脏毒性和致心律失常作用[5]；患者的心率、收缩压和舒张压也并未受显著影响，未出现与治疗相关的晕厥。与其他ASO一样，CDR132L吸收速度快，目标组织中的消除半衰期为数周，即使多次给药后随着时间的推移也未见组织积累效应。另外，miR-132抑制剂可与心衰患者的常用药物联合使用，包括肝素、血管紧张素转化酶抑制药、肾上腺素β受体阻滞药、硝酸盐、他汀类药物、阿司匹林、氯吡格雷，使慢性心衰患者的临床受益更广。
小结
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目前支持miR-132抑制剂作为心衰潜在治疗方法的证据主要来自动物模型和Ⅰb阶段临床研究，miR-132抑制剂是否可以降低缺血性心衰患者的住院率和死亡率，并改善非缺血性心衰患者的心脏重构，仍有待进一步研究。其作为一种新型抗心衰药物，在转化到临床应用之前，还需要积累更多关于其适应证以及长期安全性的证据。但miR-132抑制剂治疗心血管疾病的潜力巨大，在慢性心衰领域具有广泛的临床开发潜力，可能改变心衰患者的治疗模式，为心衰人群带来福音。
基金
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  • 甘肃省重点研发计划(20YF8FA079)
文献
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参考文献 引证文献
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2024年第43卷第1期
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doi: 10.14109/j.cnki.xyylc.2024.01.04
  • 接收时间：2022-04-27
  • 首发时间：2026-03-19
  • 出版时间：2024-01-25
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  • 收稿日期：2022-04-27
  • 录用日期：2023-05-03
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甘肃省重点研发计划(20YF8FA079)
作者信息
    1.兰州大学第一临床医学院，甘肃 兰州　730000
    2.兰州大学第一医院 老年心血管科，甘肃 兰州　730000

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