Objective:

To review recent advances in understanding intercellular communication networks involved in cardiac fibrosis, moving beyond traditional single-cell approaches.

Approach:

• Review of Intercellular Communication: The article analyzes the interactions among various cell types in the heart, including cardiomyocytes, endothelial cells, and immune cells, and their roles in fibrosis through different signaling mechanisms.
• Molecular Mechanisms: It delves into the molecular mechanisms of communication modes, clarifying the functional outcomes of each signaling pathway in fibrosis initiation and persistence.
• Therapeutic Strategies: The review examines the latest therapeutic strategies and potential intervention targets, focusing on specific cytokines, signaling pathways, and vesicular delivery systems.

Key Findings:

• Cardiac fibrosis is driven by a network of intercellular communication rather than solely by cardiac fibroblasts.
• Signaling mediators from the pericardial space play a crucial role in regulating intercellular cross-talk.
• Abnormal intercellular communication leads to excessive ECM deposition, myocardial stiffness, and cardiac dysfunction.
• Immune cells, particularly macrophages, significantly contribute to the fibrotic signaling network.

Interpretation:

The findings emphasize the need to understand interactions among different cell types in the heart.

Limitations:

• The review emphasizes the need for multi-target combined strategies, indicating limitations in single-target interventions.

Conclusion:

The exploration provides new theoretical foundations and directions for developing precise and effective anti-fibrotic therapies.