ReviewFrontiers in medicine2015
The Elusive Antifibrotic Macrophage.
Review in Frontiers in medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed, 72 citations in OpenAlex.
- Antifibrotic monocyte activation by nanoparticles resolves murine pulmonary fibrosis.Biomaterials · 2026Article
- Broad-Spectrum Protective Effects of Lyophilized FE002-Lu Lung Fibroblast Conditioned Medium Against Acute and Chronic Pulmonary Injury in Wistar Rats.Biomedicines · 2026Article
- Mechanobiology and Resolution of Lung Fibrosis.Annual review of physiology · 2026Review
- Investigating the foreign body response and regenerative mechanisms in medical-grade polycaprolactone scaffold guided breast reconstruction in a porcine model.Frontiers in bioengineering and biotechnology · 2026Article
- Antifibrotic therapies for metabolic dysfunction-associated steatotic liver disease.JHEP reports : innovation in hepatology · 2025Review
- M2 Macrophages-Based Immunotherapy: A New Therapeutic Approach in Liver Fibrosis.Advanced pharmaceutical bulletin · 2025Review
- Role of Macrophage Polarization in Chronic Rhinosinusitis Based on the Yin-Yang Theory: A Review.Journal of inflammation research · 2025Review
- Macrophage MST1 protects against schistosomiasis-induced liver fibrosis by promoting the PPARγ-CD36 pathway and suppressing NF-κB signaling.PLoS pathogens · 2024Article
- ROS-degradable polythioketal urethane scaffold for porcine wound repair.Acta pharmaceutica Sinica. B · 2024Article
- Cutting Edge: Hepatic Stellate Cells Drive the Phenotype of Monocyte-derived Macrophages to Regulate Liver Fibrosis in Metabolic Dysfunction-associated Steatohepatitis.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- The role of RNA m6A demethylase ALKBH5 in the mechanisms of fibrosis.Frontiers in cell and developmental biology · 2024Review
- Article
- Loss of SENP3 mediated the formation of nasal polyps in nasal mucosal inflammation by increasing alternative activated macrophage.Immunity, inflammation and disease · 2023Article
- Relaxin in fibrotic ligament diseases: Its regulatory role and mechanism.Frontiers in cell and developmental biology · 2023Review
- Harnessing Biomaterials for Immunomodulatory-Driven Tissue Engineering.Regenerative engineering and translational medicine · 2023Review
- Mitochondrial interaction of fibrosis-protective 5-methoxy tryptophan enhances collagen uptake by macrophages.Free radical biology & medicine · 2022Article
- Fatty acid nitroalkene reversal of established lung fibrosis.Redox biology · 2022Article
- Receptor Specificity Engineering of TNF Superfamily Ligands.Pharmaceutics · 2022Review
- Myeloid cell diversification during regenerative inflammation: Lessons from skeletal muscle.Seminars in cell & developmental biology · 2021Review
- Macrophage-stroma interactions in fibrosis: biochemical, biophysical, and cellular perspectives.The Journal of pathology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrotic diseases, especially of the liver, the cardiovascular system, the kidneys, and the lungs, account for approximately 45% of deaths in Western societies. Fibrosis is a serious complication associated with aging and/or chronic inflammation or injury and cannot be treated effectively yet. It is characterized by excessive deposition of extracellular matrix (ECM) proteins by myofibroblasts and impaired degradation by macrophages. This ultimately destroys the normal structure of an organ, which leads to loss of function. Most efforts to develop drugs have focused on inhibiting ECM production by myofibroblasts and have not yielded many effective drugs yet. Another option is to stimulate the cells that are responsible for degradation and uptake of excess ECM, i.e., antifibrotic macrophages. However, macrophages are plastic cells that have many faces in fibrosis, including profibrotic behavior-stimulating ECM production. This can be dependent on their origin, as the different organs have tissue-resident macrophages with different origins and a various influx of incoming monocytes in steady-state conditions and during fibrosis. To be able to pharmacologically stimulate the right kind of behavior in fibrosis, a thorough characterization of antifibrotic macrophages is necessary, as well as an understanding of the signals they need to degrade ECM. In this review, we will summarize the current state of the art regarding the antifibrotic macrophage phenotype and the signals that stimulate its behavior.
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Registered trials
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.