Toxic Effect of Mycotoxins on Cardiovascular System: A Topic Worthy of Further Study

ABSTRACT

Mycotoxin-caused myocardial injury has been demonstrated based on epidemiological and experimental studies. Citreoviridin (CIT) is a toxin from yellow-green Penicillium easily grown in wet and cold environment. The CIT-contaminated food intake could cause myocardial injury, which might be the etiology of endemic Keshan disease. The yellow mildewed rice could produce toxic CIT and induced beriberi-linked cardiac insufficiency. In view of the similarity between Keshan disease and cardiac beriberi (wet beriberi), it was considered that the two diseases might be the same illness with different names. Research data in recent years demonstrated that the CIT and other mycotoxins might be also associated with the vascular endothelial damage and the pathogenesis of atherosclerosis. The mycotoxin could trigger oxidative stress, free radical production, and abnormal energy metabolism in cardiomyocytes, which resulted in cell death through necrotic and apoptotic mechanisms. The mitochondrial pathway in myocardium played a critical role in mycotoxin-caused cytotoxicity. Importantly, the mycotoxins caused cell damage in vascular endothelium, which was a direct risk factor in the pathogenesis of atherosclerosis. Obviously, it is a new topic to elaborate the role of mycotoxins in the pathogenic mechanism of cardiovascular disease. There are a lot of questions needs to be answered in future study.

KEYWORDS:

• Mycotoxin
• citreoviridin
• cardiovascular disease
• myocardial injury
• Keshan disease
• mitochondrial damage
• beriberi
• cytotoxicity

List of abbreviations

CIT, citreoviridin; ATP, adenosine triphosphate; ICAM-1, intercellular adhesion molecule-1; VCAM-1, vascular cell adhesion molecule-1; VEGF, vascular endothelial growth factor; ET-1, endothelin-1; NF-κB, nuclear factor-kappa B; MCP-1, monocyte chemoattractant protein-1; IL-1β, interleukin-1β; IL-6, interleukin-6; IL-8, interleukin-8; Cyto c, cytochrome c; IAPs, inhibitors of apoptosis proteins; ROS, reactive oxygen species; ER stress, endoplasmic reticulum stress; PPARα, peroxisome proliferator-activated receptor alpha; PPARγ, peroxisome proliferator-activated receptor gamma.

Acknowledgments

This work was supported by “National Natural Science Foundation of China”, project number 81773367. We thank professor Yang Jianbo’s suggestion and advice in the preparation of manuscript.

Declaration of interests

The author(s) have nothing to disclose.

Additional information

Funding

This work was supported by the National Natural Science Foundation of China [81773367].