Exploring the cardiotoxic potential of fumonisin B1 through inflammatory pathways and epigenetic modifications: A mini review

This review is centered around the cardiotoxic effects of fumonisin B1 (FB1), particularly its impact on sphingolipid metabolism, inflammation, and epigenetics. FB1 is a mycotoxin produced by Fusarium fungi, which mainly contaminates cereal grains and poses an adverse health risk to both humans and animals; however, its disease-causing capabilities remain to be uncovered, specifically its ability to exacerbate and cause cardiovascular disease. It disrupts sphingolipid metabolism by inhibiting ceramide synthase, leading to cellular dysfunction and contributes to conditions such as hypertension and eventual heart failure. FB1 is responsible for an altered inflammatory response, whereby it increases pro-inflammatory cytokines such as IL-6 and IL-1β, which contribute to cardiovascular diseases. Moreover, FB1 induces significant epigenetic changes, including DNA hypermethylation, histone modifications such as increased H3K9me2 and H3K9me3, inhibition of histone acetyltransferase activity, and changes in microRNA expression profiles. These epigenetic alterations can silence or activate inflammatory genes, exacerbating disease progression. This review thus highlights the need for further research to elucidate the connections between FB1, inflammation, epigenetic modifications, and cardiotoxicity, which could lead to better strategies for managing FB1-related adverse health risks.