Hughes Siân E
Department of Histopathology, Royal Free and University College Medical School, University College London, UCL Hospitals NHS Trust, London, UK.
J Pathol. 2003 Oct;201(2):181-6. doi: 10.1002/path.1447.
The role of apoptosis and the methods used for its detection in failing human hearts are controversial. Recent data have challenged the hypothesis that in situ markers for DNA strand breaks mirror apoptotic (TUNEL and Taq in situ ligation assay) and/or necrotic (Pfu in situ ligation assay) cell death, and thus provide evidence that apoptotic cell loss contributes to the progression of heart failure. Experimental data cast doubt not only upon the specificity of the TUNEL technique but also the Taq in situ ligation assay as a reliable method for the detection of apoptotic cell death and provide compelling new evidence that the occurrence of cardiomyocyte cell death as defined by the detection of DNA strand breaks using either TUNEL or Taq and Pfu in situ ligation assays is an epiphenomena that is not related to the evolution of heart failure. Cardiomyocyte positivity for in situ markers of DNA strand breaks is a feature of hypertrophic cardiomyopathic hearts, irrespective of the underlying pathology or the presence or absence of heart failure. These data raise concerns regarding the extent of apoptosis in cardiomyopathy and the contribution of this process to the progression of heart failure.
细胞凋亡在衰竭的人类心脏中的作用及其检测方法存在争议。最近的数据对以下假设提出了挑战：DNA链断裂的原位标记反映凋亡（末端脱氧核苷酸转移酶介导的缺口末端标记法和Taq原位连接测定法）和/或坏死（Pfu原位连接测定法）细胞死亡，因此提供了证据表明凋亡性细胞丢失促成心力衰竭的进展。实验数据不仅对末端脱氧核苷酸转移酶介导的缺口末端标记法的特异性提出质疑，也对Taq原位连接测定法作为检测凋亡性细胞死亡的可靠方法提出质疑，并提供了令人信服的新证据，即使用末端脱氧核苷酸转移酶介导的缺口末端标记法或Taq和Pfu原位连接测定法检测DNA链断裂所定义的心肌细胞死亡的发生是一种与心力衰竭进展无关的附带现象。DNA链断裂原位标记的心肌细胞阳性是肥厚型心肌病心脏的一个特征，与潜在病理或心力衰竭的存在与否无关。这些数据引发了对心肌病中细胞凋亡程度及其在心力衰竭进展中作用的关注。
