On the one hand, myocardial FFAR3 activated by SCFAs, such as propionic acid, upregulates several pro-inflammatory (IL-1β, IL-6, activated p38 MAPK) [32] and pro-fibrotic (e.g., TGFβ [26]) factors, which is highly likely to lead to exacerbated adverse remodeling in the presence of a cardiac insult, such as myocardial ischemia/infarction or pressure overload/severe hypertension (Figure 5). The gene discussed is IL1B; the disease is infarction.