ReviewApoptosis : an international journal on programmed cell death2023
Regulation of alveolar macrophage death in pulmonary fibrosis: a review.
Review in Apoptosis : an international journal on programmed cell death, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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
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
33 citing papers in PubMed, 42 citations in OpenAlex.
- Clinical investigation on nebulized human umbilical cord MSC-derived extracellular vesicles for pulmonary fibrosis treatment.Signal transduction and targeted therapy · 2025Trial
- Progressive suppression of regulated cell death defines terminal macrophage states in liver cirrhosis.Annals of medicine · 2026Article
- Involvement of lysosomal proteins in morphology-driven toxicity of (nano)fibers.Archives of toxicology · 2026Review
- Targeting the PPAR-γ-ABC transporter axis ameliorates secondary pulmonary alveolar proteinosis induced by indium oxide nanoparticles.Particle and fibre toxicology · 2026Article
- IL-17B protects against uropathogenicMicrobiology spectrum · 2026Article
- Targeting pyroptosis to treat aortic aneurysms: From mechanism to drug discovery (Review).International journal of molecular medicine · 2026Review
- Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Disparate periphery and lung immune microenvironments induced monocyte-macrophage activation as a key factor in anti-synthetase syndrome-associated interstitial lung disease.Respiratory research · 2026Article
- Oxidized mtDNA Contributes to Pulmonary Inflammation and Fibrosis in Bleomycin-Induced Lung Injury.MedComm · 2026Article
- Identification and Functional Validation of PTH2R as a Therapeutic Target in Lung Adenocarcinoma.Biomedicines · 2026Article
- Review
- The interplay of ferroptosis and oxidative stress in pulmonary fibrosis: from mechanisms to treatment.Frontiers in cell and developmental biology · 2026Review
- Integrated long-read transcriptomic profiling of peripheral blood from ankylosing spondylitis patients identifies regulatory shifts and core genes associated with programmed cell death.Frontiers in immunology · 2026Article
- Pyroptosis, A Double-Edged Sword in Respiratory Diseases: A Narrative Review.Journal of inflammation research · 2026Review
- The crosstalk between autophagy and ferroptosis in pulmonary fibrosis.Journal of biomedical research · 2025Article
- [Itaconic acid alleviates macrophage PANoptosis in sepsisZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Article
- To Evaluate Interdisciplinary Integration in Medical Education Through a Pulmonary Fibrosis Case Study.Advances in medical education and practice · 2025Article
- Iron Overload-induced Ferroptosis as a Target for Protection against Obliterative Bronchiolitis after Orthotopic Tracheal Transplantation in Mice.Current molecular medicine · 2025Article
- Friend or foe: the role of platelets in acute lung injury.Frontiers in immunology · 2025Review
- Macrophage-Derived Exosomal BMPR2 Mediates Alveolar Epithelial Repair and Cellular Crosstalk in Acute Lung Injury.Journal of inflammation research · 2025Article
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 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary fibrosis (PF) is a disease in which excessive extracellular matrix (ECM) accumulation occurs in pulmonary mesenchyme, which induces the destruction of alveolar structures and poor prognosis. Macrophage death is responsible for ECM accumulation after alveolar epithelial injury in PF. Depending on the local micro-environments, macrophages can be polarized to either classically activated (M1) or alternatively activated (M2) macrophage phenotypes. In general, M1 macrophages can promote inflammation and sterilization, stop the continuous damage process and prevent excessive repair, while M2 macrophages are anti-inflammatory and promote tissue repair, and excessive M2 macrophage activity may inhibit the absorption and degradation of ECM. Emerging evidence has revealed that death forms such as pyroptosis mediated by inflammasome affect polarization direction and ultimately lead to the development of PF. Pharmacological manipulation of macrophages death signals may serve as a logical therapeutic strategy for PF. This review will focus on the current state of knowledge regarding the regulation and underlying mechanisms of macrophages and their mediators in the influence of macrophage death on the development of PF. We expect to provide help in developing effective therapeutic strategies in clinical settings.
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What OpenQuestion 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 OpenQuestion graph.