Microplastic Exposure Aggravates Cardiomyopathy Under Hemodynamic Stress Through the Gut-Heart Axis

Area of Science:

• Environmental Health
• Toxicology
• Microbiome Research

Background:

• Bisphenol F (BPF) is a widespread plastic chemical, often replacing Bisphenol A.
• The cardiovascular and intestinal effects of BPF are not well understood.
• This study investigates BPF's impact on the cardiovascular system and intestinal barrier.

Purpose of the Study:

• To investigate the effects of Bisphenol F (BPF) on cardiovascular health and intestinal barrier integrity.
• To explore the role of gut microbiota in BPF-induced toxicity.
• To identify the metabolic pathways and mechanisms underlying BPF toxicity.

Main Methods:

• Utilized germ-free mouse models and fecal microbiota transplantation.
• Employed untargeted and spatial metabolomics to identify BPF metabolites.
• Applied single-cell sequencing to determine affected cardiac cell types.

Main Results:

• BPF exposure, contingent on gut microbiota, caused cardiomyocyte hypertrophy, cardiac dysfunction, and intestinal barrier damage.
• Identified microbial conversion of BPF to N-acetylputrescine (NAP) via spermidine/spermine N1-acetyltransferase 1 (Sat1).
• NAP disrupted the Golgi-mitochondria axis in the intestine and activated the p53 pathway in the heart, while Akkermansia muciniphila and tryptophol showed protective effects.

Conclusions:

• BPF disrupts intestinal barrier function and causes cardiotoxicity through a novel gut microbiota-Sat1-NAP pathway.
• NAP production leads to organelle damage and cardiac hypertrophy.
• Findings offer new insights for BPF risk assessment and potential therapeutic interventions.