This paper discusses the role of cardiac fibroblasts (CF) in myocardial remodeling, focusing on their functions in regulating the extracellular matrix (ECM) and their responses to various stimuli. CF are the most abundant cell type in the heart and play a key role in maintaining normal myocardial function and in adverse remodeling associated with hypertension, myocardial infarction, and heart failure. CF can differentiate into myofibroblasts (myoFb), which express contractile proteins and exhibit increased migratory, proliferative, and secretory properties. MyoFb respond to proinflammatory cytokines, vasoactive peptides, and hormones, and their function is modulated by mechanical stretch and changes in oxygen availability. MyoFb respond to these stimuli by altering cell proliferation, migration, ECM metabolism, and secretion of bioactive molecules. Several classes of cardiovascular drugs, including ACE inhibitors, beta-blockers, statins, and thiazolidinediones, exert pleiotropic effects on CF that may explain their beneficial outcomes on the remodeling heart. The paper reviews the properties of CF, including their origin, electrophysiological properties, role in matrix metabolism, functional responses to environmental stimuli, and ability to secrete bioactive molecules. It also discusses the evidence suggesting that certain cardiovascular drugs can reduce myocardial remodeling specifically via modulatory effects on CF. The importance of CF in both physiological and pathological myocardial remodeling is highlighted, as well as their unique properties compared to fibroblasts from other tissues. The paper concludes that CF are a potentially appealing therapeutic target for the treatment of the failing heart.This paper discusses the role of cardiac fibroblasts (CF) in myocardial remodeling, focusing on their functions in regulating the extracellular matrix (ECM) and their responses to various stimuli. CF are the most abundant cell type in the heart and play a key role in maintaining normal myocardial function and in adverse remodeling associated with hypertension, myocardial infarction, and heart failure. CF can differentiate into myofibroblasts (myoFb), which express contractile proteins and exhibit increased migratory, proliferative, and secretory properties. MyoFb respond to proinflammatory cytokines, vasoactive peptides, and hormones, and their function is modulated by mechanical stretch and changes in oxygen availability. MyoFb respond to these stimuli by altering cell proliferation, migration, ECM metabolism, and secretion of bioactive molecules. Several classes of cardiovascular drugs, including ACE inhibitors, beta-blockers, statins, and thiazolidinediones, exert pleiotropic effects on CF that may explain their beneficial outcomes on the remodeling heart. The paper reviews the properties of CF, including their origin, electrophysiological properties, role in matrix metabolism, functional responses to environmental stimuli, and ability to secrete bioactive molecules. It also discusses the evidence suggesting that certain cardiovascular drugs can reduce myocardial remodeling specifically via modulatory effects on CF. The importance of CF in both physiological and pathological myocardial remodeling is highlighted, as well as their unique properties compared to fibroblasts from other tissues. The paper concludes that CF are a potentially appealing therapeutic target for the treatment of the failing heart.