Why the study?
Oxidative stress and resulting DNA double-strand breaks may be associated with sudden cardiac death, but the potential role of myocardial γ-H2AX expression as a sudden cardiac death biomarker required evaluation.
Does myocardial immunohistochemical expression of γ-H2AX differ between patients suffering sudden cardiac death and healthy controls?
Does myocardial immunohistochemical expression of γ-H2AX differ between patients suffering sudden cardiac death and healthy controls?
This study investigates the potential of γ-H2AX as a biomarker for sudden cardiac death by evaluating its myocardial immunohistochemical expression.
γ-H2AX may mark DNA damage in SCD tissues; leaves open oxidative stress as SCD driver.
Sudden cardiac death (SCD) is defined as death due to cardiovascular or unidentifiable causes that occurs within an hour of the onset of symptoms. Several lines of evidence suggest that oxidative stress, which is due to an increased production/accumulation of reactive oxygen species (ROS) in cells, may be associated with SCD. ROS can induce DNA damage leading to DNA double-strand break (DSB) that, if not repaired, can lead to cell death. In presence of a DNA DSB, H2AX (a histone H2A variant) is phosphorylated to form γ-H2AX, which binds the DNA DSBs and recruits DNA repair proteins. If DNA damage is excessive and cannot be repaired, cells undergo apoptosis. In the present study, we sought to evaluate the myocardial immunohistochemical expression of γ-H2AX in samples from patients suffering SCD as well as from healthy controls, in order to assess its potential role as a SCD biomarker.
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Tossetta et al. (2025) studied this question.
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