Propionic acid/FBP1 is involved in polystyrene nanoplastic-induced cardiac injury via the gut-heart axis

Micro-/nanoplastics (MNPLs) are widely found in the environment and have toxic effects on various organs and systems. However, the role of the gut-cardiac axis in cardiotoxicity induced by MNPLs has not yet been elucidated through research.

In this study, we examined the effects of 80 nm polystyrene nanoplastics (PS-NPs) on the heart and human cardiomyocytes (AC16) cells. Histopathological examination showed that NPs caused impaired cardiac function and increased myocardial collagen deposition. In view of the potential influence of gut microbiota and its metabolites on cardiac function, we conduct this study to investigate the specific effects they have on cardiac function. Analysis of cecal contents by 16 s ribosomal RNA (rRNA) and short chain fatty acids (SCFAs) revealed that colonic tissue damage, intestinal flora disorder, and reduction of propionic acid induced by PS-MPs were closely related to cardiac function. Further transcriptomic analysis of heart and colon tissues indicated that propionic acid may reduce cardiac function by reducing the expression of fructose-1, 6-biphosphatase 1 (FBP1). The hypothesis was further verified by in vitro intervention experiments with sodium propionate and FBP1 activator (BML-275).

In summary, our study systematically demonstrated the role of gut-heart axis in NPs-induced cardiac injury, and the specific process was that NPs exposure reduced propionate level, which in turn inhibited FBP1 expression to impair cardiac function. These findings provide new insights into NPs-induced cardiotoxicity and identifie potential therapeutic targets, providing clues for the prevention and treatment of NPs-induced cardiac injury in the future.