...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Archives of Toxicology >Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets
【24h】

Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets

机译：心脏肥大和心力衰竭的病理生理学：信号通知途径和新型治疗靶

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The onset of heart failure is typically preceded by cardiac hypertrophy, a response of the heart to increased workload, a cardiac insult such as a heart attack or genetic mutation. Cardiac hypertrophy is usually characterized by an increase in cardiomyocyte size and thickening of ventricular walls. Initially, such growth is an adaptive response to maintain cardiac function; however, in settings of sustained stress and as time progresses, these changes become maladaptive and the heart ultimately fails. In this review, we discuss the key features of pathological cardiac hypertrophy and the numerous mediators that have been found to be involved in the pathogenesis of cardiac hypertrophy affecting gene transcription, calcium handling, protein synthesis, metabolism, autophagy, oxidative stress and inflammation. We also discuss new mediators including signaling proteins, microRNAs, long noncoding RNAs and new findings related to the role of calcineurin and calcium-/calmodulin-dependent protein kinases. We also highlight mediators and processes which contribute to the transition from adaptive cardiac remodeling to maladaptive remodeling and heart failure. Treatment strategies for heart failure commonly include diuretics, angiotensin converting enzyme inhibitors, angiotensin II receptor blockers and beta-blockers; however, mortality rates remain high. Here, we discuss new therapeutic approaches (e.g., RNA-based therapies, dietary supplementation, small molecules) either entering clinical trials or in preclinical development. Finally, we address the challenges that remain in translating these discoveries to new and approved therapies for heart failure.
机译：心力衰竭的开始通常是心脏肥大，心脏响应增加工作量，心脏损伤如心脏病发作或遗传突变。心脏肥大通常是体育细胞尺寸的增加和室壁壁的增厚。最初，这种生长是保持心脏功能的适应性响应;然而，在持续压力的环境中，随着时间的推移，这些变化变得适应不足，心脏最终失败了。在本文中，我们讨论了病理心脏肥大和众多介质的关键特征，这些介质已被发现参与影响基因转录的心脏肥大，钙处理，蛋白质合成，代谢，自噬，氧化应激和炎症的发病机制。我们还讨论了新的介质，包括信号蛋白，MicroRNA，长的非编码RNA和与钙磷酸钙和钙调蛋白依赖性蛋白激酶有关的新发现。我们还突出显示介导和过程，这些过程有助于从适应性心脏重塑转变为适应心脏重塑和心力衰竭。心力衰竭的治疗策略通常包括利尿剂，血管紧张素转化酶抑制剂，血管紧张素II受体阻滞剂和β-阻滞剂;但是，死亡率仍然很高。在这里，我们讨论新的治疗方法（例如，基于RNA的疗法，膳食补充剂，小分子），要么进入临床试验或临床前发育。最后，我们解决了将这些发现转化为新的和批准的心力衰竭疗法的挑战。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号