In our study, the upregulation of cardiac FGF5, FGF7, FGF10, FGF16, and FGF18 in aged mice suggests their critical roles in aging-associated cardiac adoptive responses, whereas their reduction in aged-mice with HFD feeding indicates a disruption of this adoptive mechanism, potentially accelerating metabolic syndrome-induced cardiac damage and remodeling. Here, FGF16 is linked to metabolic syndrome.