We read with great interest the article by Li et al,¹ who demonstrated that the upregulation of ATF3, a cardiac fibroblast–enriched transcription factor, is cardioprotective against hypertensive fibrosis via suppression of Map2K3 expression and p38 MAPK signaling. Specifically, they showed that ATF3 is upregulated in cardiac fibroblasts but not in cardiomyocytes from hypertensive animals and patients with heart failure. ATF3 knockout exaggerated whereas ATF3 overexpression ameliorated ventricular remodeling in hypertensive mice. Their data strongly suggest that upregulation of ATF3 in cardiac fibroblasts is a self-compensatory protective mechanism against ventricular remodeling associated with heart failure. It is important …

我们非常感兴趣地阅读了Li等人的文章[ ^1]，他证明ATF3（一种富含心脏成纤维细胞的转录因子）的上调通过抑制Map2K3表达和p38 MAPK信号传导，对高血压纤维化具有心脏保护作用。具体而言，他们表明，ATF3在心脏成纤维细胞中被上调，但在高血压动物和心力衰竭患者的心肌细胞中则未上调。ATF3基因敲除被夸大了，而ATF3过表达改善了高血压小鼠的心室重构。他们的数据强烈表明，心脏成纤维细胞中ATF3的上调是一种自我补偿性保护机制，可防止与心力衰竭相关的心室重构。这很重要 …