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Fibrotic diseases encompass a range of pathological conditions characterized by the abnormal growth of connective tissue, involving various cell types and intricate signaling pathways. Central to the onset and development of fibrosis are macrophages and fibroblasts, whose interactions are a pivotal area of investigation. Macrophages facilitate the activation, growth, and collagen production of fibroblasts, doing so either directly or indirectly through the release of cytokines, chemokines, and growth factors. Conversely, fibroblasts boost macrophage activity and intensify local inflammatory responses by secreting cytokines and matrix proteins associated with fibrosis. Throughout the different phases of fibrosis, these two cell types communicate via cytokines and signaling pathways, thereby sustaining the pathological condition. This review emphasizes the interplay between macrophages and fibroblasts and their contributions to fibrosis in the lungs, liver, kidneys, and other organs. Furthermore, it delves into potential therapeutic targets within these interactions, with the aim of shedding light on future clinical research and treatment approaches for fibrotic diseases.
Su et al. (Wed,) studied this question.