ArticleCellular & molecular immunology2025
Targeting Lp-PLA2 inhibits profibrotic monocyte-derived macrophages in silicosis through restoring cardiolipin-mediated mitophagy.
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Article in Cellular & molecular immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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24citing papers in PubMed
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Who cites it
24 citing papers in PubMed.
- How extracellular vesicles contribute to pulmonary fibrosis: miRNA-mediated mechanisms, diagnostic potential, and emerging therapeutic strategies.Molecular biology reports · 2026Review
- Silica Nanoparticles Elicit Pulmonary Inflammation via STING-Dependent Activation of NF-κB p65 Signaling Pathway.Biomolecules · 2026Article
- SIRT6-Mediated Deacetylation of ATF3 Promotes Silica-Induced Lung Fibrosis by Enhancing its Nuclear Import via Binding to Importin α.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Mitochondrial lipid remodeling in sepsis-associated acute kidney injury: a cardiolipin-centered convergence framework.Archives of toxicology · 2026Review
- Multi-omics reveals a novel Cxcr4Clinical and translational medicine · 2026Article
- Exploring the role of RCEO in macrophage-mediated modulation of pulmonary fibrosis.Chinese medicine · 2026Article
- Integrated transcriptomic analysis identifies liver aging-driven fibrosis signatures and reveals therapeutic strategies based on medicine-food homology.NPJ science of food · 2026Article
- Phospholipase A2 Isoforms in Lung Immunity and Respiratory Infections: Potential Targets for Next-Generation Therapy.International journal of molecular sciences · 2026Review
- Profibrotic macrophage populations and cell communications in pulmonary fibrosis.Journal of physiology and biochemistry · 2026Review
- Orcinol glucoside ameliorates pulmonary fibrosis by suppressing hyaluronic acid synthesis and macrophage M2 polarization via targeting hyaluronic acid synthase 2.International journal of molecular medicine · 2026Article
- Macrophage-Derived Ferritin Exacerbates Silica-Induced Pulmonary Fibrosis via PIK3R2-Mediated Fibroblast Differentiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Persistent histone H3K27 acetylation contributes to excessive scar formation after spinal cord injury through the regulation of microglial cholesterol accumulation.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Neonatal Hyperoxia Induces Metabolic Reprogramming in Senescent Alveolar Macrophages, Leading to Persistent Lung Injury.Frontiers in bioscience (Landmark edition) · 2026Article
- Rubiadin-1-methyl ether alleviates bleomycin induced pulmonary fibrosis.Scientific reports · 2026Article
- Tools of the trade: leveraging 3DFrontiers in pharmacology · 2026Review
- Macrophage duality in liver diseases: heterogeneity, plasticity, and the quest for precision therapeutics.Frontiers in immunology · 2026Review
- SSO targets CD36 to regulate lipid metabolism disorders and improve SiOCurrent research in toxicology · 2026Article
- Targeting immunometabolism in cancer through pharmacological and lifestyle interventions.PLoS biology · 2026Review
- Exploring the effects of moxibustion on pathological remodeling in rats with myocardial ischemia-reperfusion injury based on mitochondrial cardiolipin protection.Frontiers in pharmacology · 2026Article
Corrections and comments
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Authors and funding
15 authors.
Shifeng LiNational Center for Respiratory Medicine, State Key Laboratory of Respiratory Health and Multimorbidity, National Clinical Research Center for Respiratory Diseases, Institute of Respiratory Medicine, Chinese Academy of Medical Sciences, Department of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, Beijing, China.
Hong XuHealth Science Center, Hebei Key Laboratory of Organ Fibrosis, North China University of Science and Technology, Tangshan, Hebei, China.ORCID 0000-0002-3655-3833
Shupeng LiuSchool of Public Health, Hebei Key Laboratory of Organ Fibrosis, North China University of Science and Technology, Tangshan, Hebei, China.
Jinkun HouNational Center for Respiratory Medicine, State Key Laboratory of Respiratory Health and Multimorbidity, National Clinical Research Center for Respiratory Diseases, Institute of Respiratory Medicine, Chinese Academy of Medical Sciences, Department of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, Beijing, China.
Yueyin HanNational Center for Respiratory Medicine, State Key Laboratory of Respiratory Health and Multimorbidity, National Clinical Research Center for Respiratory Diseases, Institute of Respiratory Medicine, Chinese Academy of Medical Sciences, Department of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, Beijing, China.
Chen LiNational Center for Respiratory Medicine, State Key Laboratory of Respiratory Health and Multimorbidity, National Clinical Research Center for Respiratory Diseases, Institute of Respiratory Medicine, Chinese Academy of Medical Sciences, Department of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, Beijing, China.
Yupeng LiNational Center for Respiratory Medicine, State Key Laboratory of Respiratory Health and Multimorbidity, National Clinical Research Center for Respiratory Diseases, Institute of Respiratory Medicine, Chinese Academy of Medical Sciences, Department of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, Beijing, China.
Gaigai ZhengSchool of Public Health, Hebei Key Laboratory of Organ Fibrosis, North China University of Science and Technology, Tangshan, Hebei, China.
Zhongqiu WeiBasic Medical College, Hebei Key Laboratory of Organ Fibrosis, North China University of Science and Technology, Tangshan, Hebei, China.
Fang YangSchool of Public Health, Hebei Key Laboratory of Organ Fibrosis, North China University of Science and Technology, Tangshan, Hebei, China.
Shuwei GaoNational Center for Respiratory Medicine, State Key Laboratory of Respiratory Health and Multimorbidity, National Clinical Research Center for Respiratory Diseases, Institute of Respiratory Medicine, Chinese Academy of Medical Sciences, Department of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, Beijing, China.
Shiyao WangNational Center for Respiratory Medicine, State Key Laboratory of Respiratory Health and Multimorbidity, National Clinical Research Center for Respiratory Diseases, Institute of Respiratory Medicine, Chinese Academy of Medical Sciences, Department of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, Beijing, China.
Jing GengNational Center for Respiratory Medicine, State Key Laboratory of Respiratory Health and Multimorbidity, National Clinical Research Center for Respiratory Diseases, Institute of Respiratory Medicine, Chinese Academy of Medical Sciences, Department of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, Beijing, China. jing_geng@foxmail.com.
Huaping DaiNational Center for Respiratory Medicine, State Key Laboratory of Respiratory Health and Multimorbidity, National Clinical Research Center for Respiratory Diseases, Institute of Respiratory Medicine, Chinese Academy of Medical Sciences, Department of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, Beijing, China. daihuaping@ccmu.edu.cn.
Chen WangNational Center for Respiratory Medicine, State Key Laboratory of Respiratory Health and Multimorbidity, National Clinical Research Center for Respiratory Diseases, Institute of Respiratory Medicine, Chinese Academy of Medical Sciences, Department of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, Beijing, China. cyh-birm@263.net.
Funding
China Postdoctoral Science Foundation 2023M733985National Natural Science Foundation of China (National Science Foundation of China) No. 81870056National Natural Science Foundation of China (National Science Foundation of China) No. 82003406National Natural Science Foundation of China (National Science Foundation of China) No. 82370072National Natural Science Foundation of China (National Science Foundation of China) No. 9206810167
Abstract
Monocyte-derived macrophages (MoMacs) are the most important effector cells that cause pulmonary fibrosis. However, the characteristics of MoMac differentiation in silicosis and the mechanisms by which MoMacs affect the progression of pulmonary fibrosis remain unclear. Integration of single-cell and spatial transcriptomic analyses revealed that the silicosis niche was occupied by a subset of MoMacs, identified as Spp1
Indexed as
1-Alkyl-2-acetylglycerophosphocholine EsteraseCardiolipinsMacrophagesMitophagySilicosisAnimalsHumansLysosomesMaleMiceMitochondriaPulmonary FibrosisSignal TransductionSilicon Dioxide1-Alkyl-2-acetylglycerophosphocholine EsteraseCardiolipinsPLA2G7 protein, humanSilicon DioxideCardiolipinLipoprotein-associated phospholipase A2MitophagyMonocyte-derived macrophagesPulmonary fibrosis
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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.