Figure 1: T3 has both genomic and nongenomic effects on the cardiac myocyte. Genomic effects involve binding of T3 to TRs, which in turn, positively or negatively regulates the transcription of specific cardiac genes. Nongenomic mechanisms include direct modulation of membrane ion channels.
AC = adenylyl cyclase; β-AR = β-adrenergic receptor; Ca2+ = calcium ions; Ca2+ ATPase = sarcoplasmic reticulum calcium adenosine triphosphatase; cAMP = cyclic adenosine monophosphate; GS = stimulatory G (guanine nucleotide binding) protein; K+ = potassium ions; Kv = voltage-gated potassium ion channel; mRNA = messenger ribonucleic acid; Na-K ATPase = sodium-potassium adenosine triphosphatase; Na+ = sodium ions; NCX = sodium calcium exchanger; PLB = phospholamban; T3 = triiodothyronine; TR = thyroid hormone receptor; TRE = thyroid hormone response element.