The epidermal growth factor (EGF) receptor family network in cardiac hypertrophy and heart failure

Afatinib worsened angiotensin II–induced cardiac dysfunction at 7d in mice, linked to inhibited cardiomyocyte hypertrophy and enhanced cardiac fibrosis.

• Why it matters: The EGFR family network is implicated in hypertrophy and cardioprotection, but its cell-specific dysregulation in human heart failure and its functional role in developing hypertrophy were unclear.
• What they did: Mining Human Protein Atlas data showed EGFR family receptors and EGFR-Ls are expressed in different cardiac cells, and EGFR-L mRNAs were modulated in failing versus non-failing human hearts; rat cardiomyocytes showed ligand-specific ERK1/2 and Akt activation.
• The result: In mice treated with angiotensin II for 3–7d, EGFR-L mRNAs were modulated, and at 7d afatinib/AngII produced greater dysfunction with reduced hypertrophy and increased fibrosis, supporting network involvement in hypertrophy development.