Cellular origins of atherosclerosis: towards ontogenetic endgame?
Cellular origins of atherosclerosis: towards ontogenetic endgame?
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DOI：
10.1096/fj.02-0913hyp
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发表时间：
2003-04-01
期刊：
影响因子：
4.8
通讯作者：
Rajavashisth, TB
中科院分区：
文献类型：
--
作者：
Doherty, TM;Shah, PK;Rajavashisth, TB
传统智慧已经成功地详细记录了动脉损伤后导致动脉粥样硬化斑块形成和新内膜增殖的病理过程的复杂相互作用。不幸的是，从传统智慧中衍生出来的传统疗法，在影响两种结果方面取得的成功要少得多。以动脉粥样硬化为基础的疾病造成了巨大的人力和财力损失，未来的道路看起来很严峻：随着抗生素在世界欠发达地区的使用加速，心血管疾病将很快超过感染，成为全世界死亡和残疾的主要原因（1,2）。可以肯定的是，已经取得了一些明显的胜利，比如他汀类药物治疗在改善心血管预后方面的效果。但为什么我们对病理的理解与我们对其长期影响的可测量性影响之间存在不匹配？现在也许是时候重新思考关于动脉粥样硬化本质的基本概念了。
Conventional wisdom has successfully chronicled in exquisite detail the complex interplay of pathologic processes leading to the formation of atherosclerotic plaque and neointimal proliferation after arterial injury. Conventional therapy spawned from conventional wisdom has, unhappily, achieved considerably less notable success affecting outcomes of both. Atherosclerosis-based diseases exact a tremendous human and fiscal toll, and the road ahead looks grim: as antibiotic usage in underdeveloped areas of the world accelerates, cardiovascular disease will soon overtake infection as the leading cause of death and disability in the entire world (1, 2). To be sure, there have been some clear wins, such as in the case of the efficacy of statin therapy in improving cardiovascular outcomes. But why the mismatch between our understanding of the pathology and our ability to measurably affect its long-term impact? It may now be time to rethink fundamental conceptions regarding the nature of atherosclerosis.