The role of the bidirectional regulatory network between immune cells and stromal cells in cardiac repair and fibrosis following myocardial infarction
By
Fuyuan Zhang
Yiying Liu
Ruikang Liu
Baohua Li
Jun Li
June 17, 2026
Clinical Scorecard: The Interplay Between Immune and Stromal Cells in Cardiac Repair and Fibrosis After Myocardial Infarction
At a Glance
Category Detail
Condition Key Mechanisms Bidirectional dialogue between immune cells and cardiac stromal cells, involving cytokines and chemokines. Target Population Care Setting
Key Highlights
Approximately 20-30% of acute MI survivors develop heart failure within 1–5 years. Cardiac repair is a dynamic, bidirectionally interacting cellular network. Neutrophils exhibit dual roles in cardiac repair, influencing inflammation and tissue damage. N1 and N2 neutrophil subsets play distinct roles in the inflammatory response post-MI. Guideline-Based Recommendations
Diagnosis
Monitor for signs of heart failure in acute MI survivors. Management
Focus on understanding the immune-stromal cell interactions. Monitoring & Follow-up
Assess the progression of cardiac remodeling and fibrosis post-MI. Risks
Increased mortality risk associated with heart failure following MI. Patient & Prescribing Data
Survivors of acute myocardial infarction.
Targeting the immune-matrix axis may provide new therapeutic avenues.
Clinical Best Practices
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