{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:54:41Z","timestamp":1787018081165,"version":"build-2736575974"},"reference-count":63,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","license":[{"start":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T00:00:00Z","timestamp":1783987200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2026,7,14]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>Bisphenol F (BPF) is a common substitute for bisphenol A and the most prevalent bisphenol compound in diverse plastic manufacturing applications. However, the potential toxicity of BPF remains largely unexplored. This study investigates the effects of BPF on the cardiovascular system and intestinal barrier.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>Germ-free mouse models and fecal microbiota transplantation techniques were used to confirm the role of gut microbiota in BPF-induced cardiovascular injury. Untargeted metabolomics and spatial metabolomics were used to identify the in vivo metabolic products of BPF. Single-cell sequencing was used to identify which cardiac cell types were damaged by BPF exposure.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      BPF was detected in 90.5% of 285 human urine samples (median, 1.16 ng\/\u03bcg creatinine). BPF exposure induced cardiomyocyte hypertrophy, cardiac dysfunction, and intestinal barrier damage, effects contingent on the presence of gut microbiota. Metabolomic analysis identified the microbial conversion of BPF to N-acetylputrescine (NAP). Mechanistically, we found that BPF stimulated intestinal epithelial cells to secrete spermidine\/spermine N1-acetyltransferase 1 (Sat1), which catalyzed this conversion. Furthermore, NAP impaired the intestinal barrier by disrupting the Golgi-mitochondria axis and caused cardiac hypertrophy by activating the p53 pathway and inhibiting glycolysis in cardiomyocytes. Supplementation with\n                      <jats:italic toggle=\"yes\">Akkermansia muciniphila<\/jats:italic>\n                      or its metabolite tryptophol mitigated BPF-induced cardiac and intestinal injuries by downregulating the Sat1-NAP axis. Clinical analysis further showed elevated serum NAP levels in patients with inflammatory bowel disease, positively correlating with cardiac injury markers.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>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\u2013Sat1\u2013NAP pathway underlying BPF-induced cardiotoxicity, offering new insights for risk assessment and therapeutic intervention.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circulationaha.126.079820","type":"journal-article","created":{"date-parts":[[2026,5,28]],"date-time":"2026-05-28T09:00:16Z","timestamp":1779958816000},"page":"96-116","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":1,"title":["Microplastic Exposure Aggravates Cardiomyopathy Under Hemodynamic Stress Through the Gut-Heart Axis"],"prefix":"10.1161","volume":"154","author":[{"given":"Jing","family":"Wang","sequence":"first","affiliation":[{"name":"School of Public Health (J.W., H.M., G.N., S.W., X.Z., J.Z., Q.M., R.C.)."},{"name":"Beijing Key Laboratory of Environment and Aging (J.W., Q.M., R.C.), Capital Medical University, Beijing, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4031-7531","authenticated-orcid":true,"given":"Jie","family":"Xu","sequence":"additional","affiliation":[{"name":"Yunnan Provincial Key Laboratory of Public Health and Biosafety and School of Public Health, Kunming Medical University, China (J.X.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6095-8809","authenticated-orcid":true,"given":"Huanzhuo","family":"Mai","sequence":"additional","affiliation":[{"name":"School of Public Health (J.W., H.M., G.N., S.W., X.Z., J.Z., Q.M., R.C.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-4598-6486","authenticated-orcid":true,"given":"Guolei","family":"Niu","sequence":"additional","affiliation":[{"name":"School of Public Health (J.W., H.M., G.N., S.W., X.Z., J.Z., Q.M., 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R.C.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2619-1656","authenticated-orcid":true,"given":"Michael","family":"Aschner","sequence":"additional","affiliation":[{"name":"Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY (M.A.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0003-3929-6507","authenticated-orcid":true,"given":"Qingtao","family":"Meng","sequence":"additional","affiliation":[{"name":"School of Public Health (J.W., H.M., G.N., S.W., X.Z., J.Z., Q.M., R.C.)."},{"name":"Beijing Key Laboratory of Environment and Aging (J.W., Q.M., R.C.), Capital Medical University, Beijing, China."},{"name":"Basic-Clinical Collaborative Laboratory for Colorectal Cancer Immunotherapy (Q.M.), Capital Medical University, Beijing, China."},{"name":"General Surgery Department, Xuanwu Hospital (Q.M.), Capital Medical University, Beijing, 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