Gut microbiota-induced elevation of succinate exacerbates diabetic myocardial ischemia/reperfusion injury by promoting macrophage polarization - Scorecard - MDSpire

Gut microbiota-induced elevation of succinate exacerbates diabetic myocardial ischemia/reperfusion injury by promoting macrophage polarization

  • By

  • Yang Wu

  • Juan Dou

  • Min Liu

  • Song Peng

  • Wenyuan Li

  • June 10, 2026

  • 0 min

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Clinical Scorecard: Microbiota-Derived Succinate Elevation Aggravates Myocardial Ischemia/Reperfusion Injury in Diabetic Models Through Macrophage Polarization

At a Glance

CategoryDetail
Condition
Key Mechanisms
Target PopulationDiabetic patients, particularly those with type 2 diabetes, at risk for myocardial ischemia/reperfusion injury.
Care Setting

Key Highlights

  • Diabetes increases susceptibility to myocardial ischemia/reperfusion injury.
  • Gut microbiota-derived succinate exacerbates myocardial injury through macrophage polarization.
  • Antibiotic-mediated depletion of gut microbiota reverses succinate accumulation.
  • SUCNR1 signaling pathway is critical in mediating the effects of succinate on macrophages.
  • Targeting microbial succinate production may offer therapeutic strategies.
  • Macrophage polarization plays a significant role in myocardial injury outcomes.

Guideline-Based Recommendations

Diagnosis

  • Assess gut microbiota composition and succinate levels in diabetic patients using specific diagnostic criteria.

Management

  • Consider interventions targeting succinate accumulation and macrophage polarization.

Monitoring & Follow-up

  • Monitor succinate levels and macrophage polarization markers in diabetic patients.

Risks

  • Increased myocardial injury and mortality in diabetic patients due to succinate accumulation.

Patient & Prescribing Data

Exogenous succinate supplementation may worsen myocardial injury; caution is advised.

Clinical Best Practices

  • Evaluate the role of gut microbiota in diabetic patients with cardiovascular disease.
  • Implement specific strategies to modulate macrophage polarization in myocardial injury.

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