Cardiac fibroblasts (CF) are the most prevalent cell type in the heart and play a crucial role in regulating normal myocardial function and in the adverse myocardial remodeling that occurs with conditions such as hypertension, myocardial infarction, and heart failure. CF can differentiate into myofibroblasts (myoFb), which exhibit increased migratory, proliferative, and secretory properties. MyoFb respond to various stimuli, including proinflammatory cytokines, vasoactive peptides, and hormones, which are often elevated in the remodeling heart. These stimuli modulate CF function by altering cell proliferation, migration, extracellular matrix (ECM) metabolism, and secretion of bioactive molecules. Therapeutic agents for cardiovascular disease, such as anti-hypertensives, lipid-lowering drugs, and insulin sensitizers, exert pleiotropic effects on CF, contributing to their beneficial outcomes in the remodeling heart. The review provides insights into the properties of CF, including their origin, electrophysiological properties, role in ECM metabolism, functional responses to environmental stimuli, and ability to secrete bioactive molecules. It also discusses the evidence that certain cardiovascular drugs can reduce myocardial remodeling by modulating CF function.Cardiac fibroblasts (CF) are the most prevalent cell type in the heart and play a crucial role in regulating normal myocardial function and in the adverse myocardial remodeling that occurs with conditions such as hypertension, myocardial infarction, and heart failure. CF can differentiate into myofibroblasts (myoFb), which exhibit increased migratory, proliferative, and secretory properties. MyoFb respond to various stimuli, including proinflammatory cytokines, vasoactive peptides, and hormones, which are often elevated in the remodeling heart. These stimuli modulate CF function by altering cell proliferation, migration, extracellular matrix (ECM) metabolism, and secretion of bioactive molecules. Therapeutic agents for cardiovascular disease, such as anti-hypertensives, lipid-lowering drugs, and insulin sensitizers, exert pleiotropic effects on CF, contributing to their beneficial outcomes in the remodeling heart. The review provides insights into the properties of CF, including their origin, electrophysiological properties, role in ECM metabolism, functional responses to environmental stimuli, and ability to secrete bioactive molecules. It also discusses the evidence that certain cardiovascular drugs can reduce myocardial remodeling by modulating CF function.