MIPS3526

Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.

Cardiac morphometry is based on quantitative histological and stereological assessment of myocardial structure, including cardiomyocyte size, number, and extracellular matrix composition, to evaluate cardiac growth and remodeling under physiological or pathological conditions. Design-based stereology is considered a reference framework for obtaining unbiased estimates of structural parameters such as cardiomyocyte number, volume, and tissue architecture, enabling quantitative comparison across experimental groups. Histological image-based morphometry further enables measurement of cardiomyocyte cross-sectional area and collagen deposition using microscopy combined with image analysis software, allowing assessment of hypertrophy and fibrosis in cardiac remodeling models. These morphometric readouts reflect underlying biological processes such as cardiomyocyte hypertrophy, loss, or structural reorganization during disease progression or experimental stress.