ArticleNature communications2022
Understanding fibrosis pathogenesis via modeling macrophage-fibroblast interplay in immune-metabolic context.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 61 citations in OpenAlex.
- Macrophage polarization plasticity in pulmonary fibrosis: a review from pathogenesis to therapeutic targeting.Inflammopharmacology · 2026Review
- Immune-stromal interactions at the crossroads of tissue injury, repair, and tumor progression.Med (New York, N.Y.) · 2026Review
- Review
- Identification of a personalized eGFR threshold improves the prediction of kidney failure risk after transplantation.Communications medicine · 2026Article
- Fibrosis-memory is mediated by IL-3-producing T cells and drives progression of fibrosis.The Journal of clinical investigation · 2026Article
- Quantifying Information Exchange Between Cells in Inflammaging.Bioengineering (Basel, Switzerland) · 2026Article
- Temporal tissue dynamics from a spatial snapshot.Nature · 2026Article
- Single-cell analysis of the synovium and infrapatellar fat pad identifies key pathogenic genes and drug targets in osteoarthritis.International journal of clinical and experimental pathology · 2026Article
- Role of Scar-Associated Macrophages in Organ Fibrosis Diseases.Journal of immunology research · 2026Review
- Article
- Photobiomodulation Reduces Fibrous Scar Formation After Spinal Cord Injury by Downregulating CXCL3 Expression in Macrophages.Molecular neurobiology · 2025Article
- Regulation of Tissue Regeneration by Immune Microenvironment-Fibroblast Interactions.International journal of molecular sciences · 2025Review
- The spatial and temporal activation of macrophages during fibrosis.Nature reviews. Immunology · 2025Review
- D-glucuronyl C5-Epimerase Binds to EGFR to Suppress Kidney Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Dissecting the mechanisms of MASLD fibrosis in the era of single-cell and spatial omics.The Journal of clinical investigation · 2025Review
- A fibroblast-centric network drives cold fibrosis in the tumor microenvironment of lung squamous cell carcinoma.bioRxiv : the preprint server for biology · 2025Article
- Identification of M2 macrophage-related biomarkers for a predictive model of interstitial fibrosis and tubular atrophy after kidney transplantation by machine learning algorithms.Translational andrology and urology · 2025Article
- The crucial role of metabolic reprogramming in driving macrophage conversion in kidney disease.Cellular & molecular biology letters · 2025Review
- IL-1b-Bearing NETs: Bridging Inflammation to Early Cirrhosis in Hepatitis B.International journal of molecular sciences · 2025Article
- Transcriptional Study of Radiofrequency Device Using Experimental Mouse Model.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
12 authors at 8 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrosis is a progressive biological condition, leading to organ dysfunction in various clinical settings. Although fibroblasts and macrophages are known as key cellular players for fibrosis development, a comprehensive functional model that considers their interaction in the metabolic/immunologic context of fibrotic tissue has not been set up. Here we show, by transcriptome-based mathematical modeling in an in vitro system that represents macrophage-fibroblast interplay and reflects the functional effects of inflammation, hypoxia and the adaptive immune context, that irreversible fibrosis development is associated with specific combinations of metabolic and inflammatory cues. The in vitro signatures are in good alignment with transcriptomic profiles generated on laser captured glomeruli and cortical tubule-interstitial area, isolated from human transplanted kidneys with advanced stages of glomerulosclerosis and interstitial fibrosis/tubular atrophy, two clinically relevant conditions associated with organ failure in renal allografts. The model we describe here is validated on tissue based quantitative immune-phenotyping of biopsies from transplanted kidneys, demonstrating its feasibility. We conclude that the combination of in vitro and in silico modeling represents a powerful systems medicine approach to dissect fibrosis pathogenesis, applicable to specific pathological conditions, and develop coordinated targeted approaches.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.