Key result
FMT and L-arginine supplementation reduce post-MI myocardial inflammation and fibrosis in mice.
Why the study?
Does fecal microbiota transplantation or systemic L-arginine supplementation reduce post-infarction cardiac inflammation and myocardial fibrosis in a murine model of myocardial infarction?
Does fecal microbiota transplantation or systemic L-arginine supplementation reduce post-infarction cardiac inflammation and myocardial fibrosis in a murine model of myocardial infarction?
Identifies the gut microbiota-arginine-immune axis as a critical regulator of post-MI healing in mice, suggesting microbiota-directed therapy or L-arginine supplementation as potential strategies to mitigate adverse ventricular remodeling.
Answers are grounded in this paper and cite their sources.
Gut microbiota shifts post-MI may influence inflammation; leaves open whether targeting improves cardiac repair.
Myocardial infarction (MI) triggers a robust inflammatory response that critically dictates the trajectory of cardiac repair, making the modulation of immune cells a vital therapeutic target. While the gut-heart axis is increasingly recognized in cardiovascular diseases, the upstream gut-derived signals regulating post-infarction immunity remain incompletely understood. This study aimed to characterize the dynamic changes in gut microbiota and metabolite profiles post-MI and investigate their role in cardiac inflammation and fibrosis. Using a murine model of MI, the study integrated 16 S rRNA sequencing, untargeted metabolomics, flow cytometry, and histological analyses. MI induced severe intestinal barrier dysfunction and progressive gut dysbiosis, significantly depleting Desulfovibrionaceae and Helicobacteraceae. This microbial remodeling converged on a profound reduction in both intestinal and circulating arginine levels. Consequently, this metabolic deficit was associated with an exacerbated accumulation of pro-inflammatory Ly6Chigh monocytes and CD80+ M1-like macrophages in the ischemic myocardium at day 3, driving extensive fibrotic remodeling by day 14. To validate this functional axis, targeted interventions were employed. Fecal microbiota transplantation (FMT) promoted partial microbial reconstitution and attenuated myocardial fibrosis in antibiotic-pretreated MI mice. Similarly, systemic L-arginine supplementation reduced the early accumulation of inflammatory myeloid populations and reduced myocardial fibrosis at day 14. Overall, the identified gut microbiota-arginine-immune axis acts as a critical determinant of infarct healing. These findings demonstrate that targeting upstream intestinal metabolic perturbations, through microbiota-directed therapies or metabolic recalibration, represents a biologically plausible strategy to mitigate adverse ventricular remodeling and heart failure after MI.
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Liu et al. (2026) studied Myocardial infarction (murine model). Fecal microbiota transplantation (FMT) or systemic L-arginine supplementation vs. Untreated or antibiotic-pretreated MI mice was evaluated on Myocardial inflammation (day 3) and fibrotic remodeling (day 14). Fecal microbiota transplantation and systemic L-arginine supplementation reduced day-3 inflammatory myeloid accumulation and attenuated day-14 myocardial fibrosis in post-MI mice.
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