Cardiac remodeling is the process by which the heart alters it’s mechanical composition and shape in order to adapt to constraints. This process may be physiological initially, but all forms of cardiac remodeling are associated with a risk of heart failure and eventual decompensation if pushed too far. Pathological forms of remodeling include post myocardial fibrosis and cardiac hypertrophy in response to pressure/volume overload states. This review ties together the various biochemical pathways relevant to pathological cardiac remodeling and potential treatments for target. In addition, biochemical cardiac markers relevant to discussed pathways will be reviewed alongside markers currently used for prognosis and severity of heart failure. Major influences that contribute to cardiac remodeling include the severity of underlying disease, recurrent ischemia, neuroendocrine activation, genotype, and pharmacological treatment. The main pathways that will be discussed include the TGFBeta (Tumor Growth Factor) SMAD2 (Mothersagainst decapentaplegic homolog 2) pathway, GATA4(GATA Binding Protein 4), nuclear factor of activated T cells (NFAT),and myocyte enhancer factor 2 (MEF2), specifically how they trigger ECM (extracellular matrix) proliferation and managethe switch of cardiac myocyte isoforms to the fetal type seen in pathological cardiac remodeling. In response tomyocardiocyte injury and necrosis the ECM plays a significant role in maladaptive remodeling. ECM turnover is regulated by collagengene expression and the balance between Matrix Metaloproteinase and Tissue Inhibitors of Matrix Metaloproteinase, which canbe used alongside traditional cardiac remodeling markers such as natriuretic peptides and troponins for an indication ofcardiac remodeling severity. Exploring the molecular mechanism behind cardiac remodeling can open new doors to therapies beyondcurrent pharmacological treatments available. Alternative early detection and diagnosis methods utilizing biochemicalmarkers besides those available can be beneficial in efforts aimed at reverse remodeling and improving survival in cardiac failure.