In mice with NASH-related cardiac dysfunction, through in vivo and in vitro approaches, this study revealed the pathogenic mechanisms, including downregulation of FXR and Treg-represented (IL-10/IL10R) signals, upregulation of inflammasomes, increase in the cardiac CD3+ T cell infiltration, increased crosstalk between dysregulated cardiac Treg cells and cardiomyocytes, increased apoptosis, and reduced proliferation, differentiation, and contraction of cardiomyocytes. The gene discussed is NR1H4; the disease is metabolic dysfunction-associated steatohepatitis.