Molecular Mechanisms of Cardiac Remodeling in Heart Failure Investigating the Role of Myocyte Hypertrophy, Fibrosis, and Inflammation in Disease Progression

Abstract

Background: Heart failure (HF) involves complex molecular mechanisms, including myocyte hypertrophy, fibrosis, and inflammation, which contribute to the progression of the disease. Understanding these mechanisms is critical for improving therapeutic strategies. Objective: This study investigates the molecular mechanisms of cardiac remodeling in heart failure, focusing on the roles of myocyte hypertrophy, fibrosis, and inflammation in disease progression. Method: A cohort of 100 patients with diagnosed heart failure was enrolled at Jalpaiguri Government Medical College from June 2023 to June 2024. Blood samples were collected for inflammatory cytokine profiling, and cardiac imaging and biopsies were performed to assess myocyte hypertrophy and fibrosis. Immunohistochemical analysis of myocardial tissue was conducted to evaluate markers of hypertrophy (GATA4, MEF2) and fibrosis (TGF-β, Collagen I). Quantitative PCR and ELISA were used to quantify mRNA and cytokine levels. Results: Our results revealed that 65% of patients exhibited significant myocyte hypertrophy with elevated GATA4 and MEF2 expression, correlating with reduced ejection fraction. Fibrosis was present in 75% of patients, with elevated Collagen I expression in myocardial tissue. Pro-inflammatory cytokines (TNF-α, IL-6) were significantly increased in 72% of patients, correlating with increased fibrosis (r = 0.82, p < 0.05) and worse clinical outcomes. Patients with higher inflammatory cytokine levels showed a 45% higher risk of progression to advanced heart failure. Conclusions: Myocyte hypertrophy, fibrosis, and inflammation are critical factors in the progression of heart failure. Targeting these pathways may offer new therapeutic approaches to slow disease progression.