ArticleCell death and differentiation2024
SLC15A3 plays a crucial role in pulmonary fibrosis by regulating macrophage oxidative stress.
Article in Cell death and differentiation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Protective effects and mechanism of resveratrol in animal models of pulmonary fibrosis: a preclinical systematic review and meta-analysis.Frontiers in pharmacology · 2025Pooled it
- Organelle Crosstalk and Metabolic Reprogramming in Idiopathic Pulmonary Fibrosis: Mechanisms and Therapeutic Implications.Cell biochemistry and function · 2026Review
- The Role of Polyphenols in Respiratory and Gut Health: From the Perspective of Gut-Lung Axis.Phytotherapy research : PTR · 2026Review
- Article
- Metabolic reprogramming in fibrosis-related diseases: underlying mechanisms and therapeutics.Molecular biomedicine · 2026Review
- Pulmonary fibrosis: Emerging targets and novel therapeutics.The Journal of international medical research · 2026Review
- Geranylgeranylacetone Alleviates Pulmonary Fibrosis in Mice by Activation of Nrf2 /HO-1/NQO1 Pathway.Cell biochemistry and biophysics · 2026Article
- Research on Therapeutic Strategy of Inhalable Cell Membrane-Coated Nanodelivery Complexes Mediating Nrf2 Pathway for Ameliorating Pulmonary Fibrosis.ACS applied materials & interfaces · 2026Article
- Oxidized mtDNA Contributes to Pulmonary Inflammation and Fibrosis in Bleomycin-Induced Lung Injury.MedComm · 2026Article
- Splenic Macrophage Activation and Disordered Heme-Iron Metabolism in a Mouse Model of Acute Hepatic Encephalopathy.International journal of molecular sciences · 2026Article
- Gut microbiota dysbiosis and metabolic abnormalities promote oxidative stress and fibrosis in idiopathic pulmonary fibrosis.Scientific reports · 2026Article
- Global burden and epidemiological determinants of pulmonary arterial hypertension among women aged 55 years and older: a GBD 2023 analysis.Frontiers in medicine · 2026Article
- Mechanism of SLC15A3 Regulating Macrophage Oxidative Stress in the Pathogenesis of Traumatic Tracheal Stenosis.Journal of inflammation research · 2026Article
- Piezo1 Upregulation in Monocyte-Derived Macrophages Impairs Post-Myocardial Infarction Cardiac Repair via Defective Efferocytosis and Enhanced Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- S100A8Frontiers in immunology · 2026Article
- CAR T cell therapy for fighting IPF: perspectives on a living drug.Frontiers in immunology · 2026Review
- Review
- METTL3/ALKBH5-Mediated N6-Methyladenosine Modification Drives Macrophage M1 Polarization via the SLC15A3-TASL-IRF5 Signaling Axis in Psoriasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Pulmonary fibrosis: from mechanisms to therapies.Journal of translational medicine · 2025Review
- Ferroptosis: the potential key roles in idiopathic pulmonary fibrosis.European journal of medical research · 2025Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a fatal and irreversible disease with few effective treatments. Alveolar macrophages (AMs) are involved in the development of IPF from the initial stages due to direct exposure to air and respond to external oxidative damage (a major inducement of pulmonary fibrosis). Oxidative stress in AMs plays an indispensable role in promoting fibrosis development. The oligopeptide histidine transporter SLC15A3, mainly expressed on the lysosomal membrane of macrophages and highly expressed in the lung, has proved to be involved in innate immune and antiviral signaling pathways. In this study, we demonstrated that during bleomycin (BLM)- or radiation-induced pulmonary fibrosis, the recruitment of macrophages induced an increase of SLC15A3 in the lung, and the deficiency of SLC15A3 protected mice from pulmonary fibrosis and maintained the homeostasis of the pulmonary microenvironment. Mechanistically, deficiency of SLC15A3 resisted oxidative stress in macrophages, and SLC15A3 interacted with the scaffold protein p62 to regulate its expression and phosphorylation activation, thereby regulating p62-nuclear factor erythroid 2-related factor 2 (NRF2) antioxidant stress pathway protein, which is related to the production of reactive oxygen species (ROS). Overall, our data provided a novel mechanism for targeting SLC15A3 to regulate oxidative stress in macrophages, supporting the therapeutic potential of inhibiting or silencing SLC15A3 for the precautions and treatment of pulmonary fibrosis.
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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.