We thank Dr Li and colleagues for their interest in and comments on our article,¹ in which we demonstrated a cell type–specific, ATF3-mediated transcriptional mechanism against hypertensive remodeling. They agreed with us that ATF3’s cardioprotective effects are cardiac fibroblast–dependent through antagonizing mitogen activated protein kinase kinase (MAP2K3)/p38-transforming growth factor-β (TGF-β) signaling. However, they raised 2 questions. First what is the importance of the cell-specific role of ATF3 in cardiac fibrosis? Second, does the ATF3-dependent mechanism have a general impact on cardiac fibrosis associated with different diseases (such as myocardium …

感谢李博士及其同事对我们的文章的关注和评论，在这篇文章¹中，我们展示了针对高血压重塑的一种细胞类型特异性ATF3介导的转录机制。他们同意我们的观点，ATF3的心脏保护作用是通过拮抗促分裂原活化蛋白激酶激酶（MAP2K3）/ p38转化生长因子-β（TGF-β）信号转导的。但是，他们提出了两个问题。首先，ATF3的细胞特异性作用在心脏纤维化中的重要性是什么？其次，ATF3依赖性机制是否会对与不同疾病（例如心肌...