Typical TGF-β signal transduction mobilizes Smad2 and Smad3 transcription factors to promote gene expression, which induces fibroblasts to activate and differentiate into myofibroblasts that secrete extracellular matrix proteins and thus controlling fibrosis.61 SIRT3 reduces cardiac hypertrophy mediated by the activation of MnSOD2 and improves myocardial fibrosis by blocking the TGF-β/Smad3 pathway.62,63 In our study, we found that 2-APQC reduced the phosphorylation expression levels of TGF-β, JNK, Smad3 and Lox. The gene discussed is SMAD3; the disease is cardiac hypertrophy.