ArticleJournal of cellular and molecular medicine2020
MCTR1 enhances the resolution of lipopolysaccharide-induced lung injury through STAT6-mediated resident M2 alveolar macrophage polarization in mice.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 39 citations in OpenAlex.
- Endothelial Senescence-Associated Secretory Signaling Promotes Macrophage Extracellular Traps Formation and Contributes to the Exacerbation of Combined Lung Injury.International journal of biological sciences · 2026Article
- Resolution of experimental malaria-associated acute respiratory distress syndrome is Alox12 independent and shows residual inflammation.Malaria journal · 2025Article
- Analysis of Stratifin Expression and Proteome Variation in a Rat Model of Acute Lung Injury.Journal of proteome research · 2025Article
- Advances in acute respiratory distress syndrome: focusing on heterogeneity, pathophysiology, and therapeutic strategies.Signal transduction and targeted therapy · 2025Review
- Laminarin Alleviates Acute Lung Injury Induced by LPS Through Inhibition of M1 Macrophage Polarisation.Journal of cellular and molecular medicine · 2025Article
- The potential of exogenous specialized pro-resolving mediators in protecting against sepsis-associated lung injury: a review.Frontiers in pharmacology · 2025Review
- A ROS-Responsive Lipid Nanoparticles Release Multifunctional Hydrogel Based on Microenvironment Regulation Promotes Infected Diabetic Wound Healing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- Stereochemistry and functions of the new cysteinyl-resolvin, 4S,5R-RCTR1, in efferocytosis and erythrophagocytosis of human senescent erythrocytes.American journal of hematology · 2023Article
- Pulsatilla Saponins Inhibit Experimental Lung Metastasis of Melanoma via Targeting STAT6-Mediated M2 Macrophages Polarization.Molecules (Basel, Switzerland) · 2023Article
- Different molecular pathways are disrupted in Pyoderma gangrenosum patients and are associated with the severity of the disease.Scientific reports · 2023Article
- Possibility of averting cytokine storm in SARS-COV 2 patients using specialized pro-resolving lipid mediators.Biochemical pharmacology · 2023Review
- Interaction Between Blood Vasculatures and Lymphatic Vasculatures During Inflammation.Journal of inflammation research · 2023Review
- Article
- Lack of STAT6 enhances murine acute lung injury through NLRP3/p38 MAPK signaling pathway in macrophages.BMC immunology · 2022Article
- Macrophage-intrinsic DUOX1 contributes to type 2 inflammation and mucus metaplasia during allergic airway disease.Mucosal immunology · 2022Article
- Molecular Pharmacology of Inflammation Resolution in Atherosclerosis.International journal of molecular sciences · 2022Review
- Specialized pro-resolving mediators as modulators of immune responses.Seminars in immunology · 2022Review
- Human leukocytes selectively convert 4Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Anti-Inflammatory Function of Fatty Acids and Involvement of Their Metabolites in the Resolution of Inflammation in Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute respiratory distress syndrome (ARDS) is a fatal disease characterized by excessive infiltration of inflammatory cells. MCTR1 is an endogenously pro-resolution lipid mediator. We tested the hypothesis that MCTR1 accelerates inflammation resolution through resident M2 alveolar macrophage polarization. The mice received MCTR1 via intraperitoneal administration 3 days after LPS stimulation, and then, the bronchoalveolar lavage (BAL) fluid was collected 24 hours later to measure the neutrophil numbers. Flow cytometry was used to sort the resident and recruited macrophages. Post-treatment with MCTR1 offered dramatic benefits in the resolution phase of LPS-induced lung injury, including decreased neutrophil numbers, reduced BAL fluid protein and albumin concentrations and reduced histological injury. In addition, the expression of the M2 markers Arg1, FIZZ1, Remlα, CD206 and Dectin-1 was increased on resident macrophages in the LPS + MCTR1 group. Resident macrophage depletion abrogated the therapeutic effects of MCTR1, and reinjection of the sorted resident macrophages into the lung decreased neutrophil numbers. Finally, treatment with MCTR1 increased STAT6 phosphorylation. The STAT6 inhibitor AS1517499 abolished the beneficial effects of MCTR1. In conclusion, MCTR1 promotes resident M2 alveolar macrophage polarization via the STAT6 pathway to accelerate resolution of LPS-induced lung injury.
Indexed as
Identifiers
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.