ArticleJournal of advanced research2025
RvD1 improves resident alveolar macrophage self-renewal via the ALX/MAPK14/S100A8/A9 pathway in acute respiratory distress syndrome.
Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 18 citations in OpenAlex.
- Alveolar Macrophages: Development, Respiratory Homeostasis, Signal Pathways, Diseases, and Therapeutic Opportunities.MedComm · 2026Review
- The Acute Respiratory Distress Syndrome (ARDS): epidemiology, etiology, molecular mechanisms, diagnosis and therapeutic strategies.Molecular biomedicine · 2026Review
- Lung microbiota-derived deoxyinosine alleviates TBI-aggravated sepsis-induced lung injury via the S100A9/RAGE pathway.Journal of neuroinflammation · 2026Article
- Estrogen receptor β deficiency increases susceptibility to sepsis through metabolic reprogramming-induced macrophage pyroptosis.The Journal of clinical investigation · 2026Article
- FGF21 promotes the resolution of inflammation through the ALOX15/SPM pathway in acute respiratory distress syndrome.Respiratory research · 2026Article
- Lipoxin A4 activates Nrf2 expression and mitigates hyperglycaemia-induced impairment of myogenesis and rescues damage to mitochondria.Journal of physiology and biochemistry · 2026Article
- Indole-acetaldehyde from Rothia mucilaginosa activates the PXR/NRF2 axis to enhance alveolar macrophage phagocytosis and protect against ARDS.Respiratory research · 2026Article
- The Transcription Factor DDIT3 Regulates Macrophage Function by Inhibiting KLF10 to Attenuate ALI/ARDS Inflammation.Inflammation · 2026Article
- Lipoxin A4 AttenuatesJournal of inflammation research · 2026Article
- From lipid switch to tissue repair: how resolvins reprogram macrophage polarization and function.Immunometabolism (Cobham, Surrey) · 2026Review
- Trends and Prospects in Inflammation Resolution in Acute Lung Injury and Acute Respiratory Distress Syndrome: A Bibliometric Quantitative and Visualization Analysis.Mediators of inflammation · 2026Article
- Gentisic acid ameliorates lumbar disc herniation by regulating M1/M2 Polarization via the MAPK14/S100A9/Rac1/2 pathway.Cell biology and toxicology · 2025Article
- Article
- Progression in the In Vitro Macrophage Expansion.Journal of immunology research · 2025Review
- Single-Cell Sequencing Redefines Immune Heterogeneity and Communication Networks in ARDS: Toward Precision Therapeutics.International journal of genomics · 2025Review
- The potential of exogenous specialized pro-resolving mediators in protecting against sepsis-associated lung injury: a review.Frontiers in pharmacology · 2025Review
- Expression and clinical significance of S100A8/9 in adults with secondary phagocytic lymphohistiocytosis.Frontiers in molecular biosciences · 2025Article
- Resolvin D1 combined with exercise rehabilitation alleviates neurological injury in mice with intracranial hemorrhage via the BDNF/TrkB/PI3K/AKT pathway.Scientific reports · 2024Article
- SS31 alleviates LPS-induced acute lung injury by inhibiting inflammatory responses through the S100A8/NLRP3/GSDMD signaling pathway.European journal of medical research · 2024Article
Corrections and comments
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Authors and funding
24 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionAcute respiratory distress syndrome (ARDS) is a pulmonary inflammatory process primarily caused by sepsis. The resolution of inflammation is an active process involving the endogenous biosynthesis of specialized pro-resolving mediators, including resolvin D1 (RvD1). Resident alveolar macrophages (RAMs) maintain pulmonary homeostasis and play a key role in the resolution phase. However, the role of RAMs in promoting the resolution of inflammation by RvD1 is unclear.
objectivesHere, we investigated the mechanisms of RvD1 on regulating RAMs to promote the resolution of ARDS.
methodsMice were administered lipopolysaccharide and/or Escherichia coli via aerosol inhalation to establish a self-limited ARDS model. Then, RvD1 was administered at the peak inflammatory response. RAMs self-renewal was measured by flow cytometry, RAM phagocytosis was measured by two-photon fluorescence imaging. In addition, plasma was collected from intensive care unit patients on days 0-2, 3-5, and 6-9 to measure RvD1 and S100A8/A9 levels using triple quadrupole/linear ion trap mass spectrometry.
resultsRAMs were found to play a pivotal role in resolving inflammation during ARDS, and RvD1 enhanced RAM proliferation and phagocytosis, which was abrogated by a lipoxin A4 receptor (ALX, RvD1 receptor) inhibitor. Both primary RAMs transfected with rS100A8/A9 and/or S100A8/A9 siRNA and S100A9
conclusionsWe propose that RvD1 improved RAM self-renewal and phagocytosis via the ALX/MAPK14/S100A8/A9 signaling pathway. Plasma RvD1 and S100A8/A9 levels were negatively correlated, and associated with the outcome of sepsis-induced ARDS.
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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.