Mitochondria-associated endoplasmic reticulum membranes and cardiac hypertrophy: Molecular mechanisms and therapeutic targets.
Mitochondria-associated endoplasmic reticulum membranes and cardiac hypertrophy: Molecular mechanisms and therapeutic targets.
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线粒体相关内质网膜和心脏肥大：分子机制和治疗靶点
DOI：
10.3389/fcvm.2022.1015722
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发表时间：
2022
影响因子：
3.6
通讯作者：
中科院分区：
文献类型：
--
作者：
心肌肥厚已被证明可以补偿心脏功能，改善室壁张力和氧耗。这种代偿反应会导致几种心脏疾病，包括缺血性疾病、高血压、心力衰竭和瓣膜疾病。尽管心肌肥厚的发病机制仍然复杂，但以往的数据表明线粒体和内质网(ER)功能障碍介导了心肌肥厚的进展。线粒体与内质网之间的相互作用是由线粒体相关内质网膜(MAM)介导的，它在心肌肥厚的病理过程中起着重要的作用。MAMs的功能主要与钙转运、脂质合成、自噬和活性氧(ROS)有关。在这篇综述中，我们讨论了关键的MAMs相关蛋白及其在心血管系统中的功能，并确定了它们在心肌肥厚进展中的作用。此外，我们还证明MAMs是治疗心肌肥厚的潜在靶点。
Cardiac hypertrophy has been shown to compensate for cardiac performance and improve ventricular wall tension as well as oxygen consumption. This compensatory response results in several heart diseases, which include ischemia disease, hypertension, heart failure, and valvular disease. Although the pathogenesis of cardiac hypertrophy remains complicated, previous data show that dysfunction of the mitochondria and endoplasmic reticulum (ER) mediates the progression of cardiac hypertrophy. The interaction between the mitochondria and ER is mediated by mitochondria-associated ER membranes (MAMs), which play an important role in the pathology of cardiac hypertrophy. The function of MAMs has mainly been associated with calcium transfer, lipid synthesis, autophagy, and reactive oxygen species (ROS). In this review, we discuss key MAMs-associated proteins and their functions in cardiovascular system and define their roles in the progression of cardiac hypertrophy. In addition, we demonstrate that MAMs is a potential therapeutic target in the treatment of cardiac hypertrophy.
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影响因子：
3.5
作者：
De Vos KJ;Mórotz GM;Stoica R;Tudor EL;Lau KF;Ackerley S;Warley A;Shaw CE;Miller CC
通讯作者：
Miller CC
影响因子：
11.4
作者：
Benham, AM;Cabibbo, A;Braakman, I
通讯作者：
Braakman, I
影响因子：
13.3
作者：
Gelmetti, Vania;De Rosa, Priscilla;Valente, Enza Maria
通讯作者：
Valente, Enza Maria
影响因子：
5.3
作者：
Gilquin, Benoit;Taillebourg, Emmanuel;Baudier, Jacques
通讯作者：
Baudier, Jacques
DOI：
10.1083/jcb.200211046
发表时间：
2003-01-20
期刊：
The Journal of cell biology
影响因子：
--
作者：
Chen H;Detmer SA;Ewald AJ;Griffin EE;Fraser SE;Chan DC
通讯作者：
Chan DC