Meanwhile, the research by Azakie et al. demonstrated that cardiac hypertrophy in a clinically relevant sheep model resulted from an increase in left-to-right shunt, left ventricular preload, and right ventricular afterload, accompanied by elevated SP1 expression and reduced SP3 expression in all four chambers, aligning with SP1 activation and SP3 inhibition of cTnT promoter activity. This evidence concerns the gene SP3 and cardiac hypertrophy.