Macrophages play a crucial role in the regulation of fibrosis, both as profibrotic and antifibrotic agents. They produce profibrotic mediators such as transforming growth factor-β1 (TGF-β1) and platelet-derived growth factor (PDGF), which activate fibroblasts and control extracellular matrix (ECM) turnover. Macrophages also regulate fibrosis by secreting chemokines that recruit fibroblasts and other inflammatory cells. The functions of macrophages in fibrosis can be both pro- and antifibrotic, depending on the context and the specific subpopulation of macrophages involved. Recent studies have identified distinct macrophage subpopulations, such as classically activated macrophages (CAMφ) and alternatively activated macrophages (AAMφ), which exhibit different phenotypes and functions. AAMφ, in particular, have been shown to have a protective role in fibrosis by modulating Th2 cytokine responses and promoting the resolution of fibrosis. Macrophages also regulate fibrosis through the production of matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs), which control ECM degradation. Additionally, macrophages can remove cellular debris and phagocytose apoptotic myofibroblasts, which helps to terminate the fibrotic process. The role of macrophages in fibrosis is complex and multifaceted, and future research aims to identify specific macrophage subpopulations and soluble mediators that can be targeted to reverse established fibrosis.Macrophages play a crucial role in the regulation of fibrosis, both as profibrotic and antifibrotic agents. They produce profibrotic mediators such as transforming growth factor-β1 (TGF-β1) and platelet-derived growth factor (PDGF), which activate fibroblasts and control extracellular matrix (ECM) turnover. Macrophages also regulate fibrosis by secreting chemokines that recruit fibroblasts and other inflammatory cells. The functions of macrophages in fibrosis can be both pro- and antifibrotic, depending on the context and the specific subpopulation of macrophages involved. Recent studies have identified distinct macrophage subpopulations, such as classically activated macrophages (CAMφ) and alternatively activated macrophages (AAMφ), which exhibit different phenotypes and functions. AAMφ, in particular, have been shown to have a protective role in fibrosis by modulating Th2 cytokine responses and promoting the resolution of fibrosis. Macrophages also regulate fibrosis through the production of matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs), which control ECM degradation. Additionally, macrophages can remove cellular debris and phagocytose apoptotic myofibroblasts, which helps to terminate the fibrotic process. The role of macrophages in fibrosis is complex and multifaceted, and future research aims to identify specific macrophage subpopulations and soluble mediators that can be targeted to reverse established fibrosis.