Similarly, there were no alterations in markers for fibrotic change (Tgfb1, Gjd3, Col1a1, and Col3a1), although there was a reduced transcription of α1B-adrenergic receptor subtypes (Adra1b) known to mediate protective and adaptive functions preventing pathological remodeling in cardiac failure through Gq/11 signaling (O’Connell et al., 2013) and of the transcriptional repressor Tbx3. There was increased transcription of the complementary Pgc-1α (Ppargc1a) involved in adjustments to altered metabolic demand. The gene discussed is COL3A1; the disease is heart failure.