Fibrosis, which is characterized by excessive extracellular matrix (ECM) deposition in the interstitium, is a major pathological consequence of chronic inflammation and contributes to progressive tissue dysfunction. Although ECM accumulation initially supports tissue repair, dysregulated wound-healing responses lead to persistent fibrotic remodeling. The development of effective anti-fibrotic therapies is limited by an incomplete understanding of the mechanisms driving fibrosis progression. Normal wound healing involves tightly coordinated processes, including platelet activation, inflammatory cell recruitment, fibroblast migration, ECM deposition, and collagen remodeling. Disruption of these events results in pathological scar formation and sustained fibrosis. This study investigated the progression of fibrotic remodeling in a myocardial infarction rat model to delineate the key biological events associated with the transition from adaptive repair to maladaptive fibrosis. Histological and molecular analyses were conducted to evaluate ECM accumulation and remodeling dynamics during disease progression. The findings provide mechanistic insights into the development of fibrosis following a myocardial infarction and identify potential therapeutic targets. These results contribute to a better understanding of pathological wound healing and support the development of strategies to attenuate fibrosis and improve cardiac outcomes.