Troponin release following brief myocardial ischemia: apoptosis versus necrosis.
Troponin release following brief myocardial ischemia: apoptosis versus necrosis.
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DOI：
10.1016/j.jacbts.2017.03.008
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发表时间：
2017-04
期刊：
影响因子：
--
通讯作者：
Kitsis RN
中科院分区：
文献类型：
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作者：
Amgalan D;Pekson R;Kitsis RN
心肌特异性肌钙蛋白I(CTnI)的释放进入体循环通常被认为是心肌细胞坏死的生物标志物，并用于心肌梗死的诊断。但是，在剧烈运动、无症状患者和急性冠脉综合征以外的疾病状态下，似乎健康的人血液cTnI浓度一过性升高(1)。后者包括不足以引起梗塞、心力衰竭、心肌炎、肺栓塞、心律失常、败血症和创伤的短暂性脑缺血发作。虽然心肌细胞死亡是这些疾病中的一部分，但它在其他情况下的参与可能不那么突出或值得怀疑。血cTnI浓度在急性冠脉综合征的临床背景下仍然是一项重要的诊断试验，但这些观察结果强调了在解释时需要注意的必要性。此外，他们提出了关于介导cTnI释放的细胞机制以及相应地它作为生物标记物的细胞过程的问题。这些问题很重要，因为血液中cTnI浓度的增加与不良心血管事件和死亡率有关。
Release of the cardiac-specific isoform of troponin I (cTnI) into the systemic circulation is frequently taken as a biomarker of cardiomyocyte necrosis and used in the diagnosis of myocardial infarction. But, transient increases in blood cTnI concentrations are observed in seemingly healthy individuals following strenuous exercise, asymptomatic patients, and disease states other than acute coronary syndromes (1). The latter include short bouts of ischemia insufficient to cause infarction, heart failure, myocarditis, pulmonary embolism, arrhythmias, sepsis, and trauma. Although cardiomyocyte death is a component of some of these conditions, its involvement in others may be less prominent or questionable. Blood cTnI concentrations remain an important diagnostic test in the clinical context of acute coronary syndromes, but these observations highlight the need for caveats in their interpretation. Moreover, they raise questions regarding the cellular mechanisms that mediate cTnI release and, accordingly, the cellular processes for which it serves as a biomarker. These questions are important because increases in blood cTnI concentrations are associated with adverse cardiovascular events and mortality.