Cardiac fibrosis: from mechanisms and models to medicines

Area of Science:

• Cardiology
• Biomedical Engineering
• Stem Cell Biology

Background:

• Cardiac fibrosis is a significant pathological feature in various cardiovascular and systemic diseases.
• Current therapeutic strategies for cardiac fibrosis are limited, with no FDA-approved treatments directly targeting fibrotic remodeling.
• Challenges in disease modeling and translation hinder the development of effective antifibrotic therapies.

Purpose of the Study:

• To review emerging molecular mechanisms driving cardiac fibrosis.
• To synthesize recent advances in experimental models for studying cardiac fibrosis.
• To consolidate findings on preclinical and clinical investigations of antifibrotic agents.

Main Methods:

• Analysis of recent literature on cardiac fibrosis mechanisms and therapeutic development.
• Focus on human induced pluripotent stem cell (iPSC)-derived models, engineered heart tissues, and in vivo systems.
• Emphasis on cross-contextual alignment of molecular drivers and therapeutic targets.

Main Results:

• Identification of novel fibrotic drivers, including immune-stroma crosstalk, metabolic reprogramming, and mechanotransduction.
• Advancements in experimental models offer improved fidelity for studying fibrotic processes.
• Emerging antifibrotic agents show promise in preclinical and clinical investigations.

Conclusions:

• New insights into fibrotic drivers are reshaping therapeutic development for cardiac fibrosis.
• Advanced models are crucial for understanding and targeting cardiac fibrosis.
• Cross-contextual alignment is key to developing precision antifibrotic therapies.