Fibrosis is a pathological process characterized by excessive deposition of extracellular matrix components, particularly collagen, leading to tissue scarring and loss of function. It arises from chronic inflammatory responses triggered by various stimuli, including infections, autoimmune reactions, and tissue injury. While current treatments for fibrotic diseases primarily target inflammation, emerging evidence suggests that fibrogenesis involves distinct mechanisms, with ongoing inflammation potentially playing a role in reversing established fibrosis. The key cellular mediator of fibrosis is the myofibroblast, which produces collagen and is derived from various sources, including resident mesenchymal cells, epithelial cells, and circulating fibrocytes. Myofibroblasts are activated by signals from immune cells, growth factors, and pathogen-associated molecular patterns. Cytokines such as IL-13, IL-21, and TGF-β1, along with chemokines and angiogenic factors, regulate fibrosis and are being explored as targets for antifibrotic therapies. The cellular origins of myofibroblasts include epithelial-mesenchymal transition, endothelial-mesenchymal transition, and fibrocytes derived from bone marrow. Innate and adaptive immune mechanisms, including TLR signaling and Th1/Th2 cytokines, regulate myofibroblast activity and fibrosis. Th2 cytokines such as IL-4, IL-5, IL-13, and IL-21 play significant roles in fibrosis, while TGF-β1 is a major profibrotic mediator. Angiotensin II also contributes to fibrosis by promoting TGF-β1 production and fibroblast activation. Endogenous mechanisms, including regulatory T cells and IL-10, can suppress fibrosis. While reversing fibrosis is challenging, recent studies suggest that it may be possible in some cases, particularly in the context of immune clearance. Antifibrotic strategies are being explored, including targeting cytokines, chemokines, and TGF-β signaling, with the goal of restoring tissue homeostasis and preventing disease progression. The development of effective antifibrotic therapies remains a critical area of research, with a focus on translating experimental findings into clinical applications.Fibrosis is a pathological process characterized by excessive deposition of extracellular matrix components, particularly collagen, leading to tissue scarring and loss of function. It arises from chronic inflammatory responses triggered by various stimuli, including infections, autoimmune reactions, and tissue injury. While current treatments for fibrotic diseases primarily target inflammation, emerging evidence suggests that fibrogenesis involves distinct mechanisms, with ongoing inflammation potentially playing a role in reversing established fibrosis. The key cellular mediator of fibrosis is the myofibroblast, which produces collagen and is derived from various sources, including resident mesenchymal cells, epithelial cells, and circulating fibrocytes. Myofibroblasts are activated by signals from immune cells, growth factors, and pathogen-associated molecular patterns. Cytokines such as IL-13, IL-21, and TGF-β1, along with chemokines and angiogenic factors, regulate fibrosis and are being explored as targets for antifibrotic therapies. The cellular origins of myofibroblasts include epithelial-mesenchymal transition, endothelial-mesenchymal transition, and fibrocytes derived from bone marrow. Innate and adaptive immune mechanisms, including TLR signaling and Th1/Th2 cytokines, regulate myofibroblast activity and fibrosis. Th2 cytokines such as IL-4, IL-5, IL-13, and IL-21 play significant roles in fibrosis, while TGF-β1 is a major profibrotic mediator. Angiotensin II also contributes to fibrosis by promoting TGF-β1 production and fibroblast activation. Endogenous mechanisms, including regulatory T cells and IL-10, can suppress fibrosis. While reversing fibrosis is challenging, recent studies suggest that it may be possible in some cases, particularly in the context of immune clearance. Antifibrotic strategies are being explored, including targeting cytokines, chemokines, and TGF-β signaling, with the goal of restoring tissue homeostasis and preventing disease progression. The development of effective antifibrotic therapies remains a critical area of research, with a focus on translating experimental findings into clinical applications.