Topic: Mechanical Overload-Induced Cardiac Remodeling

Cardiac remodeling induced by mechanical overload represents a fundamental yet complex adaptive and then maladaptive response to sustained hemodynamic stress, serving as a critical pathological substrate for numerous cardiovascular diseases. Mechanical overload is broadly categorized into pressure overload (PO) and volume overload (VO), which predominantly drive concentric and eccentric hypertrophy, respectively. While initially compensatory, prolonged mechanical stress disrupts myocardial homeostasis, leading to dysfunctional remodeling characterized by fibrosis, inflammation, and ultimately heart failure. This remodeling process is a common pathogenic pathway in conditions such as hypertension, aortic valve disease (stenosis and regurgitation), and myocardial infarction. Despite advances in our understanding, the distinct and overlapping molecular, cellular, and extracellular mechanisms underlying PO- versus VO-induced remodeling, and the translation of these insights into targeted therapies, remain areas of intense investigation and significant clinical relevance.

This Special Issue, entitled “Mechanical Overload-Induced Cardiac Remodeling,” aims to compile cutting-edge research and comprehensive reviews that dissect the multifaceted biology of cardiac remodeling under abnormal mechanical loading. We seek to bridge fundamental discoveries—spanning mechanotransduction signaling, epigenetic reprogramming, cellular crosstalk, and morphological-functional adaptations—with translational perspectives, including disease modeling, clinical correlations, and novel therapeutic strategies. By integrating knowledge from molecular and cellular studies, preclinical models, engineered tissues, and clinical observations, this Special Issue provides a platform to advance mechanistic understanding and foster the development of innovative interventions to prevent or reverse adverse remodeling, thereby improving outcomes for patients with mechanically overloaded hearts.

Recommended Subtopics:

1. Molecular Mechanisms of Mechanotransduction in Cardiomyocytes, Cardiac Fibroblasts, and Immune Cells under Pressure or Volume Overload;

2. Distinct Signaling Pathways and Cellular Outcomes in Concentric versus Eccentric Hypertrophy;

3. Epigenetic and Non-Coding RNA Regulatory Networks in the Transition from Adaptive Hypertrophy to Heart Failure;

4. Sex Differences, Aging, and Comorbidities in Cardiac Remodeling Responses to Mechanical Stress;

5. Right Ventricular Adaptation and Failure in Response to Pressure versus Volume Overload (e.g., Pulmonary Hypertension, Tricuspid Regurgitation);

6. Atrial Remodeling, Dysfunction, and Arrhythmogenesis under Chronic Mechanical Loading;

7. Novel Therapeutic Targets and Pharmacological Strategies for Specific Overload Types: From Bench to Bedside;

8. Comparative Clinical Insights and Management Strategies for Diseases Dominated by Pressure Overload (e.g., Aortic Stenosis) versus Volume Overload (e.g., Aortic Regurgitation);

9. Engineering In Vitro Models: Biomimetic Systems, Cardiac Organoids, and Advanced Culture Platforms to Mimic the Mechanical Overload Microenvironment;

10. Physiological versus Pathological Hypertrophy: Lessons from Exercise, Pregnancy, and Disease Models;

11. Multi-Organ Crosstalk in Mechanical Overload: Cardio-Renal, Cardio-Hepatic, and Neurohormonal Interactions;

12. Advanced Imaging, Biomarkers, and Computational Modeling for Assessing and Predicting Remodeling under Mechanical Overload.

Cardiac remodeling, mechanical overload, pressure overload, volume overload, concentric hypertrophy, eccentric hypertrophy, mechanotransduction, heart failure, fibrosis, epigenetic regulation