Loading
Myocardial Ischemia–reperfusion Injury / Disease Models, Animal / Fusobacterium Infections · Journal article
Gut Microbes · April 25, 2026
Encouraging direction, but not yet definitive.
This mechanistic study identifies a novel oral-gut microbiome axis whereby oral F. nucleatum reshapes gut microbial composition and elevates circulating imidazole propionate (ImP), which aggravates myocardial ischemia-reperfusion injury. The work demonstrates that F. nucleatum exerts cardiotoxic effects without persistent colonic colonization, instead altering gut Lactobacillus abundance and gut urocanate reductase-associated metabolic functions.
Journal article. Mice receiving oral F. nucleatum gavage and patients with coronary heart disease; H9c2 cells for in vitro hypoxia/reoxygenation experiments. Intervention: Oral F. nucleatum gavage in mice; imidazole propionate administration. Compared with: Antibiotic-mediated microbiota depletion; p62 knockdown versus control.
F. nucleatum aggravated MIRI despite the absence of persistent colonic colonization Antibiotic-mediated microbiota depletion reduced ImP and attenuated myocardial injury Plasma ImP was elevated in patients with CHD
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
This work identifies ImP as a potentially actionable microbial metabolite linking oral dysbiosis to cardiac injury, suggesting that targeting gut microbial metabolism rather than oral pathogens directly may offer a novel therapeutic strategy to mitigate MIRI. The findings support microbiota-based risk stratification and intervention in patients undergoing coronary revascularization.
Mechanistic study combining mouse models, patient cohorts, and cell work demonstrates a novel oral-gut microbiome axis linking F. nucleatum to myocardial injury via imidazole propionate.
As stated by the source record.
Quoted from the source exactly as published.
This work identifies ImP as a potentially actionable microbial metabolite linking oral dysbiosis to cardiac injury, suggesting that targeting gut microbial metabolism rather than oral pathogens directly may offer a novel therapeutic strategy to mitigate MIRI. The findings support microbiota-based risk stratification and intervention in patients undergoing coronary revascularization.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Background. Myocardial ischemia-reperfusion injury (MIRI) remains a major complication. Fusobacterium nucleatum (F. nucleatum), an oral pathobiont associated with cardiometabolic disease, may influence host physiology by reshaping gut microbial function through an oral-gut axis. Whether such microbial interactions contribute to MIRI remains unclear.Methods. An oral F. nucleatum gavage mouse model and cohorts were established to investigate the effect of oral F. nucleatum on MIRI, gut microbial histidine metabolism including imidazole propionate (ImP) production, the association of ImP with coronary heart disease (CHD), and its microbial sources. MIRI was induced with or without antibiotic-mediated microbiota depletion and/or ImP administration, and p62 dependence was examined by knockdown approaches in vitro and in vivo. Plasma metabolites, cardiac injury, ultrastructure, and p62/mTOR signaling were assessed.Results. F. nucleatum aggravated MIRI despite the absence of persistent colonic colonization. Instead, F. nucleatum altered gut microbial composition, including Lactobacillus abundance, and was associated with elevated circulating ImP. Antibiotic-mediated microbiota depletion reduced ImP and attenuated myocardial injury. Plasma ImP was elevated in patients with CHD, and ImP-producing capacity was supported primarily by gut microbiota urocanate reductase (UAR)-associated functions. In H9c2 cells, ImP exacerbated hypoxia/reoxygenation injury, and increased the autophagy adaptor p62 together with downstream mTOR/S6K1 signaling. p62 knockdown attenuated the mTOR/S6K1 response and injury-associated changes, whereas IRS1 suppression persisted.Conclusions. F. nucleatum reshapes gut microbial metabolism, thereby amplifying MIRI via ImP. ImP emerges as a functional mediator linking oral dysbiosis to MIRI, and reducing microbiota-derived ImP may represent a more mechanistically grounded strategy to mitigate MIRI.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.