Heart failure & cardiomyopathies
Microplastic Exposure Aggravates Cardiomyopathy Under Hemodynamic Stress Through the Gut-Heart Axis
Authors' conclusion
BPF disrupts intestinal barrier function through microbial metabolism involving the tryptophol/Sat1 pathway, leading to NAP production. NAP damages intestinal organelles and enters circulation, inducing cardiac p53 activation and hypertrophy. This study delineates a novel gut microbiota-Sat1-NAP pathway underlying BPF-induced cardiotoxicity.
Study context
- Population
- Mice and human urine samples; patients with inflammatory bowel disease
- Participants
- 285 human urine samples
- Outcome
- Effects of BPF on the cardiovascular system and intestinal barrier
Methodological detailsgerm-free mouse models, fecal microbiota transplantation, untargeted and spatial metabolomics, single-cell sequencing, human urine and serum samples
- Germ-free mouse models
- Fecal microbiota transplantation
- Untargeted and spatial metabolomics
- Single-cell sequencing
- Human urine and serum samples
Main finding
As reported in the abstract
BPF exposure, gut microbiota and cardiac/intestinal injury
Bisphenol F (BPF) detected in human urine samples
90.5% of 285
Urinary BPF, median
1.16 ng/μg creatinine
Further findings
- Elevated serum N-acetylputrescine (NAP) levels in patients with inflammatory bowel disease, positively correlating with cardiac injury markers
- Clinical analysis
Original publication
Microplastic Exposure Aggravates Cardiomyopathy Under Hemodynamic Stress Through the Gut-Heart Axis. Circulation. Published 28 May 2026. doi:10.
Summarised from the published abstract; every number is checked against it