T-2 toxin and its cardiotoxicity: New insights on the molecular mechanisms and therapeutic implications

Abstract

T-2 toxin is one of the most toxic and common trichothecene mycotoxins, and can cause various cardiovascular diseases. In this review, we summarized the current knowledge-base and challenges as it relates to T-2 toxin related cardiotoxicity. The molecular mechanisms and potential treatment approaches were also discussed. Pathologically, T-2 toxin-induced cardiac toxicity is characterized by cell injury and death in cardiomyocyte, increased capillary permeability, necrosis of cardiomyocyte, hemorrhage, and the infiltration of inflammatory cells in the heart. T-2 toxin exposure can cause cardiac fibrosis and finally lead to cardiac dysfunction. Mechanistically, T-2 toxin exposure-induced cardiac damage involves the production of ROS, mitochondrial dysfunction, peroxisome proliferator-activated receptor-gamma (PPAR-γ) signaling pathway, endoplasmic reticulum (ER stress), transforming growth factor beta 1 (TGF-β1)/smad family member 2/3 (Smad2/3) signaling pathway, and autophagy and inflammatory responses. Antioxidant supplementation (e.g., catalase, vitamin C, and selenium), induction of autophagy (e.g., rapamycin), blockade of inflammatory signaling (e.g., methylprednisolone) or treatment with PPAR-γ agonists (e.g., pioglitazone) may provide protective effects against these detrimental cardiac effects caused by T-2 toxin. We believe that our review provides new insights in understanding T-2 toxin exposure-induced cardiotoxicity and fuels effective prevention and treatment strategies against this important food-borne toxin-induced health problems.