Cellular and molecular basis of RV hypertrophy in congenital heart disease.
Cellular and molecular basis of RV hypertrophy in congenital heart disease.
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DOI：
10.1136/heartjnl-2015-308348
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发表时间：
2016-01
期刊：
影响因子：
--
通讯作者：
Tulloh RM
中科院分区：
文献类型：
--
作者：
Iacobazzi D;Suleiman MS;Ghorbel M;George SJ;Caputo M;Tulloh RM
右心室肥大 (RVH) 是先天性心脏病 (CHD) 中右心室衰竭的诱因之一。因此，提高我们对这种病理学的细胞和分子基础的理解将有助于制定战略性治疗干预措施，以提高未来患者的利益。这篇综述描述了从 RVH 到 RV 衰竭转变的潜在机制。特别是，它解决了结构和功能重塑，包括收缩功能障碍、代谢变化、基因表达变化和细胞外基质重塑。缺血应激和活性氧的产生都与触发这些变化有关，将进行讨论。最后，将讨论针对各种先心病的 RV 重塑以及生物标志物的潜在作用。
RV hypertrophy (RVH) is one of the triggers of RV failure in congenital heart disease (CHD). Therefore, improving our understanding of the cellular and molecular basis of this pathology will help in developing strategic therapeutic interventions to enhance patient benefit in the future. This review describes the potential mechanisms that underlie the transition from RVH to RV failure. In particular, it addresses structural and functional remodelling that encompass contractile dysfunction, metabolic changes, shifts in gene expression and extracellular matrix remodelling. Both ischaemic stress and reactive oxygen species production are implicated in triggering these changes and will be discussed. Finally, RV remodelling in response to various CHDs as well as the potential role of biomarkers will be addressed.