2. Academic Validation
  3. Flavonifractor Plautii or Its Metabolite Desaminotyrosine as Prophylactic Agents for Alleviating Myocardial Ischemia/Reperfusion Injury

Flavonifractor Plautii or Its Metabolite Desaminotyrosine as Prophylactic Agents for Alleviating Myocardial Ischemia/Reperfusion Injury

  • Adv Sci (Weinh). 2025 Jun;12(21):e2417827. doi: 10.1002/advs.202417827.
Heng Du 1 2,  Xu Liu 1 2,  Jianghua Shen 1 2,  Hailong Yuan 1 2,  Hao Zhang 1 2,  Gan Xi 2 3,  Yujing Li 1 2 4 5,  Yuhan Wang 1 2 4 5,  Jiahe Zhang 1 2 4 5,  Chaofan Yang 1 2 4 5,  Pengfei Xu 1 2 4 5,  Jiawan Wang 6,  Fang Wang 1 4,  Siqi Liu 1 2 4 5,  Yanan Zhou 1 2 4 5,  Qi Gu 1 2 4 5,  Jingjing Lu 2 3,  Tuo Wei 1 2 4 5,  Zeyu Gao 1 5,  Jingyi Zang 1 5,  Jun Wang 2 3,  Moshi Song 1 2 4 5
Affiliations

Affiliations

  • 1 State Key Laboratory of Organ Regeneration and Reconstruction, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
  • 2 University of Chinese Academy of Sciences, Beijing, 100049, China.
  • 3 CAS Key Laboratory of Pathogenic Microbiology and Immunology, Chinese Academy of Sciences, Beijing, 100101, China.
  • 4 Beijing Institute for Stem Cell and Regenerative Medicine, Beijing, 100101, China.
  • 5 Institute for Stem Cell and Regeneration, Chinese Academy of Sciences, Beijing, 100101, China.
  • 6 Department of Anesthesiology, Beijing Chao-Yang Hospital, Beijing, 100020, China.
PMID: 40089859 DOI: 10.1002/advs.202417827
Abstract

Myocardial ischemia/reperfusion (I/R) injury is a major contributor to myocardial damage, leading to adverse cardiac remodeling and dysfunction. Recent studies have highlighted the potential of gut microbiota-derived metabolites in modulating cardiac outcomes. Here, the cardioprotective effects of a commensal bacterium Flavonifractor plautii (F. plautii) and its metabolite desaminotyrosine (DAT) against myocardial I/R injury are investigated. We showed that prophylactic gavage of F. plautii attenuates myocardial I/R injury as evidenced by improved cardiac function and reduced cardiac injury. We also found that its metabolite DAT recapitulates these cardioprotective effects against myocardial I/R injury. Transcriptomic analysis has revealed that DAT preserves cardiac tissue and attenuates immune responses against myocardial I/R injury. Mechanistically, DAT promotes cardiomyocyte survival through the modulation of the nicotinamide adenine dinucleotide phosphate (NADP+/NADPH) ratio. Further, DAT suppressed macrophage proinflammatory activities and cardiac inflammation via the reduction in interleukin-6 (IL-6) production. Taken together, our findings indicate that F. plautii and its metabolite DAT exert pleiotropic cardioprotective effects against myocardial I/R injury, suggesting them as potential prophylactic therapeutic options for alleviating myocardial I/R injury.

Keywords

Flavonifractor plautii; cardiac inflammation; cardiomyocyte survival; desaminotyrosine; myocardial ischemia/reperfusion injury.

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