ArticleThe American journal of pathology2026
Macrophages Are Critical Inducers of Bleomycin-Induced Fibrosis in a Systemic Scleroderma Model.
Article in The American journal of pathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- Alpha-Lipoic Acid Attenuates Fibrotic and Inflammatory Dermal Remodelling in a Bleomycin-Induced Skin Model.Cell biochemistry and biophysics · 2026Article
- Antibiotic-Induced Pulmonary Fibrosis: National Database Analysis.Biomedicines · 2026Article
- Tissue-specific oxidative stress and bleomycin hydrolase signatures are associated with organ-specific fibrotic responses in a mouse model of systemic sclerosis.Frontiers in cell and developmental biology · 2026Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Macrophages are critical regulators of inflammation with an essential role in maintaining and re-establishing homeostasis after inflammatory insults. However, excessive macrophage activation could promote fibrosis, highlighting their potential as a therapeutic target in chronic inflammatory diseases. Two preclinical models of systemic sclerosis, bleomycin-induced systemic scleroderma and sclerodermatous graft-versus-host disease, were used to analyze the role of macrophages in the establishment of fibrosis. In both models, macrophage numbers increase in the skin and lungs, in association with elevated collagen content and correlating with fibrosis development. These macrophages had a Ly6c
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