I n this issue of the Journal, Tanimoto et al. (1) used recombinant heat shock protein (HSP)-72 coupled to the variable fragment (Fv) of an antibody that enables cell penetration. The fusion protein was first shown to protect cardiomyocytes from hydrogen peroxide–mediated cell death. In a rabbit model of ischemia-reperfusion, the fusion protein was administered 1 min before reperfusion, with imaging, functional, and histological readouts after 3 h of reperfusion. The authors reported reduction of Tc-annexin-V uptake in the area at risk for the Fv-HSP72 group compared with controls (Fv alone or HSP72 alone); they also observed a reduction in troponin I release in the Fv-HSP72–treated group and improved ejection fraction (measured at 3-h reperfusion). Histological analysis and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining also revealed cardioprotective effects of the fusion protein.

中文翻译：

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在本期杂志中，Tanimoto 等人。(1) 使用与抗体可变片段 (Fv) 偶联的重组热休克蛋白 (HSP)-72，使细胞能够穿透。融合蛋白首次被证明可以保护心肌细胞免受过氧化氢介导的细胞死亡。在兔缺血再灌注模型中，在再灌注前 1 分钟施用融合蛋白，再灌注 3 小时后进行成像、功能和组织学读数。作者报告说，与对照（单独的 Fv 或单独的 HSP72）相比，Fv-HSP72 组在危险区域的 Tc-膜联蛋白-V 摄取减少；他们还观察到 Fv-HSP72 治疗组的肌钙蛋白 I 释放减少，射血分数提高（在 3 小时再灌注时测量）。