Mechanistically, it inhibited the TLR4/Myd88 inflammatory pathway and upregulated the Nrf2/HO-1 antioxidant pathway.<h4>Conclusion</h4>This approach, which simultaneously targets fibrosis, inflammation, oxidative stress, and autonomic nervous system imbalance, demonstrates the potential for a multi-target therapeutic strategy against complex cardiac diseases caused by dyslipidemia. Here, MYD88 is linked to heart disorder.