The role of the bidirectional regulatory network between immune cells and stromal cells in cardiac repair and fibrosis following myocardial infarction

1

Heart failure following myocardial infarction (MI) is a major complication, with 20-30% of survivors developing heart failure within 1-5 years.
2

The cardiac repair process after MI is a dynamic interaction between immune cells and stromal cells, rather than a simple linear cascade.
3

Neutrophils play dual roles in cardiac repair, initially promoting inflammation but later aiding in tissue repair through N2 polarization.
4

The imbalance in the immune-stromal network can shift from essential repair responses to pathological fibrosis, leading to heart failure.
5

Novel therapeutic strategies targeting the immune-matrix axis are proposed to improve prevention and treatment of heart failure after MI.

Frontiers In Immunology

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