The Microenvironment of the Pathogenesis of Cardiac Hypertrophy

Area of Science:

• Cardiovascular Biology
• Cellular Signaling
• Pathophysiology

Background:

• Pathological cardiac hypertrophy is a major risk factor for heart failure, cardiac arrhythmia, and sudden death.
• Unlike adaptive physiological hypertrophy, maladaptive hypertrophy arises from conditions like hypertension, aortic stenosis, or genetic mutations (e.g., hypertrophic cardiomyopathy).
• The complex myocardial microenvironment and signaling pathways are critical in cardiac hypertrophy development.

Purpose of the Study:

• To highlight the essential roles and reciprocal interactions of cardiomyocytes and non-myocardial cells in pathological cardiac hypertrophy.
• To summarize recent advances in cardiac hypertrophy research.
• To discuss the complex myocardial microenvironment and signaling components involved.

Main Methods:

• Review of recent decades' advances in cardiac hypertrophy research.
• Analysis of signaling events triggered by cardiovascular stress.
• Integration of hypertrophic mediators into computational models.

Main Results:

• Prolonged cardiovascular stress activates cardiomyocytes and non-myocardial cells, releasing pro-hypertrophic, pro-fibrotic, and pro-inflammatory mediators.
• Cardiac fibroblasts, endothelial cells, and immune cells mediate fibrotic remodeling.
• Computational models integrating hypertrophic mediators offer system-level insights.

Conclusions:

• Reciprocal interactions between cardiomyocytes and non-myocardial cells are crucial in pathological cardiac hypertrophy.
• Understanding these complex signaling networks can lead to new pharmacological targets for treating cardiac hypertrophy and related conditions.
• This perspective synthesizes current knowledge on the myocardial microenvironment in cardiac hypertrophy.