In this regard, our results demonstrating the suppression of pro-fibrotic genes like COL1A1, COL3A1, and COL14A1 through HDAC5 inhibition are particularly significant (Figure 8), as myocardial fibrosis, characterized by excessive deposition of extracellular matrix proteins (especially collagen I and III), is a critical mechanism in heart failure progression [11]. The gene discussed is COL3A1; the disease is heart failure.