Mitral valve disease--morphology and mechanisms.
Mitral valve disease--morphology and mechanisms.
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DOI：
10.1038/nrcardio.2015.161
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发表时间：
2015-12
期刊：
影响因子：
--
通讯作者：
Leducq Mitral Transatlantic Network
中科院分区：
文献类型：
--
作者：
Levine RA;Hagége AA;Judge DP;Padala M;Dal-Bianco JP;Aikawa E;Beaudoin J;Bischoff J;Bouatia-Naji N;Bruneval P;Butcher JT;Carpentier A;Chaput M;Chester AH;Clusel C;Delling FN;Dietz HC;Dina C;Durst R;Fernandez-Friera L;Handschumacher MD;Jensen MO;Jeunemaitre XP;Le Marec H;Le Tourneau T;Markwald RR;Mérot J;Messas E;Milan DP;Neri T;Norris RA;Peal D;Perrocheau M;Probst V;Pucéat M;Rosenthal N;Solis J;Schott JJ;Schwammenthal E;Slaugenhaupt SA;Song JK;Yacoub MH;Leducq Mitral Transatlantic Network
二尖瓣病变是导致心力衰竭和死亡的常见原因。新出现的证据表明，二尖瓣不是一种被动结构，但--即使在成年生活中--仍保持着活力，可以接受治疗。这一概念促使人们努力通过早期发现和修改潜在的机制来减少二尖瓣疾病的临床进展。导致二尖瓣延长和脱垂的基因突变的发现表明，生长因子信号和细胞迁移途径受到结构分子的调控，可以通过修改的方式来限制从发育缺陷到瓣膜退变的进展并伴有临床并发症。二尖瓣扩大可以确定肥厚型心肌病左室流出道梗阻，并可能受到潜在可改变的生物瓣膜-心室相互作用的刺激。二尖瓣的可塑性也允许适应性生长，以响应心室重构。然而，在缺血环境中，不利的细胞和机械生物学过程造成相对的叶功能缺陷，导致二尖瓣返流，增加心力衰竭和死亡率。我们的方法架起了临床医生和基础科学家的桥梁，使观察到的疾病与细胞和分子机制相关联，从而发现了改善二尖瓣疾病自然病史的新机会。
Mitral valve disease is a frequent cause of heart failure and death. Emerging evidence indicates that the mitral valve is not a passive structure, but—even in adult life—remains dynamic and accessible for treatment. This concept motivates efforts to reduce the clinical progression of mitral valve disease through early detection and modification of underlying mechanisms. Discoveries of genetic mutations causing mitral valve elongation and prolapse have revealed that growth factor signalling and cell migration pathways are regulated by structural molecules in ways that can be modified to limit progression from developmental defects to valve degeneration with clinical complications. Mitral valve enlargement can determine left ventricular outflow tract obstruction in hypertrophic cardiomyopathy, and might be stimulated by potentially modifiable biological valvular–ventricular interactions. Mitral valve plasticity also allows adaptive growth in response to ventricular remodelling. However, adverse cellular and mechanobiological processes create relative leaflet deficiency in the ischaemic setting, leading to mitral regurgitation with increased heart failure and mortality. Our approach, which bridges clinicians and basic scientists, enables the correlation of observed disease with cellular and molecular mechanisms, leading to the discovery of new opportunities for improving the natural history of mitral valve disease.