Key result
Urolithin B ameliorates post-MI cardiac dysfunction by suppressing TREM1-mediated macrophage pyroptosis and promoting autophagy.
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Why the study?
Existing standard therapies for myocardial infarction have limitations such as reperfusion injury, and new intervention strategies are urgently needed.
Does Urolithin B ameliorate post-myocardial infarction cardiac dysfunction in preclinical models?
Does Urolithin B ameliorate post-myocardial infarction cardiac dysfunction in preclinical models?
Urolithin B demonstrates potential as a novel therapeutic agent for post-myocardial infarction cardiac repair by dual modulation of macrophage pyroptosis and autophagy via TREM1.
BACKGROUND Myocardial infarction is a major cause of death worldwide. The existing standard therapies have limitations such as reperfusion injury, and new intervention strategies are urgently needed. Urolithin B (UB) is a natural phytochemical with multi-target biological activity. It has high bioavailability and good safety. Preliminary preclinical evidence indicates that it can improve cardiac function, but the specific mechanism remains to be elucidated. METHODS To investigate these mechanisms, we conducted a series of in vivo and in vitro experiments to evaluate the effect of UB on myocardial cells after myocardial infarction. The differences in the levels of pyroptosis and autophagy in vivo were confirmed through bioinformatics analysis, immunofluorescence, and Western blot. The inhibitory effect of UB on pyroptosis and its promotive effect on autophagy were further demonstrated using immunofluorescence, electron microscopy, and Western blot. The downstream mechanisms of UB were explored via RNA sequencing combined with bioinformatics analysis. RESULTS Our findings revealed a significant increase in both autophagy and pyroptosis levels within myocardial infarction. Notably, treatment with UB led to a marked inhibition of macrophage pyroptosis alongside an enhancement of autophagy levels. Further investigations identified macrophage triggering receptor-1 (TREM1) as the critical downstream target of UB. TREM1 was observed to promote myocardial cell proliferation, while also activating pyroptosis and inhibiting autophagy in macrophages. CONCLUSION This study is the first to elucidate the dual modulation of autophagy and pyroptosis by UB in the context of myocardial infarction, highlighting its potential as a novel therapeutic agent. Our results suggest that UB's targeting of TREM1 may facilitate cardiac repair mechanisms, presenting a promising adjunct to conventional treatments for myocardial infarction. Future research should aim to further validate these findings and explore the clinical applicability of UB in enhancing cardiac recovery.
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Li et al. (2026) studied Myocardial infarction. Urolithin B was evaluated on Cardiac dysfunction, pyroptosis, and autophagy levels. Urolithin B ameliorated post-myocardial infarction cardiac dysfunction by inhibiting macrophage pyroptosis and enhancing autophagy through the targeting of TREM1.
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