ReviewCell death discovery2024
Macrophages in organ fibrosis: from pathogenesis to therapeutic targets.
Review in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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
69 citing papers in PubMed.
- Progressive suppression of regulated cell death defines terminal macrophage states in liver cirrhosis.Annals of medicine · 2026Article
- Ion channel/Stat6-driven nano-immune programming of tissue-resident macrophages by amide-functionalized nanocellulose.Bioactive materials · 2026Article
- Association between serum anti-granulocyte-macrophage colony-stimulating factor autoantibodies and nintedanib-induced diarrhea in interstitial lung disease: a retrospective study.Journal of thoracic disease · 2026Article
- Targeting canonical TGFβ/SMAD3 and ERK1/2 signaling in human valve interstitial cells to modulate immune-fibrotic responses in rheumatic heart disease.Journal of physiology and biochemistry · 2026Article
- Coordinated Two-Node Blockade of NF-κB and TGF-β/Smad Signaling Attenuates the Foreign Body Response to Prevent Capsular Contracture.Biomedicines · 2026Article
- Unleashing innovative cross-organ fibrosis therapies by harnessing the omics revolution.JCI insight · 2026Review
- The cell with many faces: lung macrophage plasticity and function in response to environmental and pathogenic insults.Physiological reviews · 2026Review
- Inflammation-driven mitochondrial dysfunction and ROS accumulation orchestrate pulmonary fibrotic remodeling in sepsis.Redox biology · 2026Article
- Apolipoprotein E knockout attenuates vascular graft fibrosis by reducing profibrotic macrophage formation through low-density lipoprotein receptor related protein 1.Bioactive materials · 2026Article
- In Vivo Imaging of the Innate Immune System in the Pancreas in New-Onset and Long-Standing Type 1 Diabetes.Diabetes, obesity & metabolism · 2026Article
- Surface N-Glycosylation Dictates MSC-EV Uptake and CCR2-Driven Monocyte Recruitment to Inflamed Endothelium Under Shear Flow.Journal of extracellular vesicles · 2026Article
- YAP/TAZ inhibition refines TGF-β signaling to prevent laryngeal fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Programmable synthetic cytokine receptors polarize macrophages to user-defined functional states.bioRxiv : the preprint server for biology · 2026Article
- TNFAIP3 in M2 Macrophage Attenuates Subretinal Fibrosis in Laser-Induced Murine Model.Investigative ophthalmology & visual science · 2026Article
- Defined culture conditions improve functional properties of mature iPSC-derived macrophages for therapeutic screening.Stem cell research & therapy · 2026Article
- Dysplastic Epithelial Repair Propagates Chronic Pathology Through the Paracrine Transformation of Pulmonary Fibroblasts.bioRxiv : the preprint server for biology · 2026Article
- Clonal Hematopoiesis Instructs Maladaptive Tissue Repair to Promote Fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Non-viableMicrobiology spectrum · 2026Article
- Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrosis, an excessive self-repair response, is an age-related pathological process that universally affects various major organs such as the heart, liver, kidney, and lungs. Continuous accumulation of pathological tissue fibrosis destroys structural integrity and causes loss of function, with consequent organ failure and increased mortality. Although some differences exist in the triggering mechanisms and pathophysiologic manifestations of organ-specific fibrosis, they usually share similar cascading responses and features, including chronic inflammatory stimulation, parenchymal cell injury, and macrophage recruitment. Macrophages, due to their high plasticity, can polarize into different phenotypes in response to varied microenvironments and play a crucial role in the development of organ fibrosis. This review examined the relationship between macrophages and the pathogenesis of organ fibrosis. Moreover, it analyzed how fibrosis can be modulated by targeting macrophages, which may become a novel and promising therapeutic strategy for fibrosis.
Identifiers
What Socratic holds
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 Socratic graph.