Response by Du et al to Letter Regarding Article, “Cardiac Fibroblast-Specific Activating Transcription Factor 3 Protects Against Heart Failure by Suppressing MAP2K3-p38 Signaling”
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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 …