Immune-stromal imbalance drives heart failure after myocardial infarction, systematic review findsImmune cell balance determines if heart tissue heals or fails
Frontiers in MedicinePublished June 18, 2026Study authors: Fuyuan Zhang, Yiying Liu, Ruikang Liu, Baohua Li, Jun LiDOI ↗Editorial oversight: Dr. Amelia Tan, PhD · Internal Medicine & Chronic Disease
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Key Takeaway
Consider the immune-stromal network as a potential target for preventing heart failure after MI, but note the lack of clinical data.
This systematic review synthesizes evidence on the bidirectional regulatory network between immune cells (neutrophils, macrophages, lymphocytes) and stromal cells (cardiac fibroblasts, endothelial cells, pericytes) during spatiotemporal evolution following myocardial infarction (MI). The review maps complex interactive networks and identifies that an imbalance in the immune-matrix network shifts from essential repair responses to pathological fibrosis, ultimately leading to heart failure.
Key findings include that the immune-stromal interaction is critical for cardiac repair, fibrosis, and inflammation resolution. However, when the network is disrupted, pathological fibrosis ensues, contributing to heart failure development. The review does not provide pooled effect sizes or quantitative results, as it is a descriptive synthesis of biological interactions.
Limitations are not reported in the source, and the review is based on theoretical frameworks and mapping of biological interactions without clinical trial data or specific drug efficacy results. The authors aim to provide new perspectives for precise prevention and treatment of heart failure after MI by targeting the immune-matrix axis.
Practice relevance is restrained: the findings offer a conceptual foundation but require validation in clinical studies before translation to patient care.
How this fits prior evidence
This systematic review extends prior coverage by providing a mechanistic framework for heart failure after MI. It complements findings on engineered extracellular vesicles for cardiac repair by detailing the cellular interactions that may underlie such therapies. It also contrasts with clinical trials of digoxin and finerenone, which focus on pharmacological interventions, by highlighting the immune-stromal axis as a potential target. The review addresses a gap in understanding the transition from repair to fibrosis, which is not directly addressed by telemedicine or antithrombotic strategies.
After a heart attack, the body works hard to repair damaged muscle. However, not every heart heals the same way. Some people recover well, while others develop heart failure. Scientists are looking closer at how immune cells and structural cells in the heart work together to find out why this happens.
This review mapped the complex ways that immune cells, like macrophages and lymphocytes, interact with the heart's supporting tissue. They found that a specific balance is needed for healing. When this communication between immune cells and the heart's framework becomes unbalanced, the body stops repairing the muscle and starts creating excessive scar tissue, known as fibrosis.
This research provides a new roadmap for doctors to understand the underlying biology of heart failure. By focusing on this interaction between immune cells and the heart's structure, researchers hope to find better ways to prevent permanent damage after a heart attack. While this study maps out biological pathways rather than testing specific drugs, it offers a new foundation for future treatments.
What this means for you:
An imbalance in how immune cells talk to heart tissue can turn necessary repair into permanent heart failure.
Common questions
What causes heart failure after a heart attack?
Heart failure can happen when the communication between immune cells and the heart's structural cells becomes unbalanced. Instead of focusing on repairing the damaged muscle, the body begins to create excessive scar tissue, which is called fibrosis. This shift from repair to scarring makes it harder for the heart to pump blood effectively.
What role do immune cells play in heart repair?
Immune cells like macrophages and lymphocytes work with structural cells to manage inflammation and repair tissue after a heart attack. The research shows these cells must interact correctly over time. When they stay balanced, the heart can heal; when they become unbalanced, it leads to lasting damage.
Heart failure following myocardial infarction (MI) is a major complication affecting long-term prognosis of patient, with its core pathological processes being ventricular pathological remodeling and fibrosis. This process is not merely simple scar formation, but is dominated by a continuous, dynamic, and intricate bidirectional dialogue between immune cells and cardiac stromal cells. This review systematically mapped the complex interactive networks between immune cells—including neutrophils, macrophages, and lymphocytes—and stromal cells such as cardiac fibroblasts, endothelial cells, and pericytes during the spatiotemporal evolution following MI. We emphasizes the key communication pathways involving cytokines, chemokines, fibrotic signals, and active signals from the microenvironment. And we mappied their spatiotemporal network governing the initiation and resolution of inflammation and fibrosis. Simultaneously, we explored how this network’s imbalance shifts from essential repair responses to pathological fibrosis, ultimately leading to heart failure. Furthermore, we summarized novel therapeutic strategies targeting the immune-matrix axis, aiming to provide new perspectives and theoretical foundations for the precise prevention and treatment of heart failure following MI.
