Key result
Single-cell transcriptomics reveals macrophage diversity in organ fibrosis extends far beyond the traditional M1/M2 dichotomy.
Why the study?
Organ fibrosis causes approximately 45% of global mortality and lacks effective clinical treatments, with macrophage heterogeneity in fibrosis not fully characterized beyond the M1/M2 paradigm.
Provides a contemporary framework for understanding macrophage heterogeneity in organ fibrosis using single-cell and spatial transcriptomics, surpassing the traditional M1/M2 paradigm.
Challenges M1/M2-centric fibrosis therapies; leaves open validation of conserved SPP1+ subsets for cardiac targeting.
Organ fibrosis is the ultimate common pathway resulting from dysregulated tissue repair caused by chronic inflammation, it accounts for approximately 45% of global mortality, and there are currently no effective clinical treatments to reverse it. As the central immune cells in the fibrotic microenvironment, macrophages exhibit a high degree of phenotypic and functional heterogeneity that far exceeds the traditional M1/M2 dichotomy. Based on the latest evidence from single-cell transcriptomics and spatial transcriptomics, this review establishes a multidimensional framework for macrophage heterogeneity that encompasses cellular origin, disease stage, spatial microenvironment, and functional output. We compared the conserved and organ-specific characteristics of macrophage subsets in pulmonary, hepatic, renal, and cardiac fibrosis, highlighting that Secreted Phosphoprotein 1
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Qiu et al. (2026) conducted a review in Organ fibrosis. Single-cell and spatial transcriptomics reveal that macrophage heterogeneity in organ fibrosis extends beyond the M1/M2 dichotomy across pulmonary, hepatic, renal, and cardiac tissues.
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