ArticleHepatology (Baltimore, Md.)2017
Expression of scavenger receptor-AI promotes alternative activation of murine macrophages to limit hepatic inflammation and fibrosis.
Article in Hepatology (Baltimore, Md.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 36 citations in OpenAlex.
- Polarization of Hepatic Macrophages in Alveolar Echinococcosis and Its Role in Remodeling the Immune Microenvironment.Tropical medicine and infectious disease · 2026Review
- Gold Nanoparticles in Atherosclerosis: A Dual Approach to Diagnosis and Therapy.Molecular imaging and biology · 2025Review
- Multi-targeted olink proteomics analyses of cerebrospinal fluid from patients with aneurysmal subarachnoid hemorrhage.Proteome science · 2024Article
- Identification of female-enriched and disease-associated microglia (FDAMic) contributes to sexual dimorphism in late-onset Alzheimer's disease.Journal of neuroinflammation · 2024Article
- The mechanism of low molecular weight fucoidan-incorporated nanofiber scaffolds inhibiting oral leukoplakia via SR-A/Wnt signal axis.Frontiers in pharmacology · 2024Article
- Damage-mediated macrophage polarization in sterile inflammation.Frontiers in immunology · 2023Review
- Macrophage polarization is involved in liver fibrosis induced by βActa biochimica et biophysica Sinica · 2022Article
- Article
- Scavenger Receptors: Novel Roles in the Pathogenesis of Liver Inflammation and Cancer.Seminars in liver disease · 2022Review
- Role of macrophage scavenger receptor MSR1 in the progression of non-alcoholic steatohepatitis.Frontiers in immunology · 2022Review
- The role of macrophage scavenger receptor 1 (MSR1) in inflammatory disorders and cancer.Frontiers in immunology · 2022Review
- A critical role for MSR1 in vesicular stomatitis virus infection of the central nervous system.iScience · 2021Article
- Macrophage Polarization and Its Role in Liver Disease.Frontiers in immunology · 2021Review
- Dysbiosis From a Microbial and Host Perspective Relative to Oral Health and Disease.Frontiers in microbiology · 2021Review
- Macrophage scavenger receptor 1 controls Chikungunya virus infection through autophagy in mice.Communications biology · 2020Article
- Transcriptomic Profiles of Monocyte-Derived Macrophages in Response to Escherichia coli is Associated with the Host Genetics.Scientific reports · 2020Article
- Phase I study of emactuzumab single agent or in combination with paclitaxel in patients with advanced/metastatic solid tumors reveals depletion of immunosuppressive M2-like macrophages.Annals of oncology : official journal of the European Society for Medical Oncology · 2019Article
- Exome-wide search and functional annotation of genes associated in patients with severe tick-borne encephalitis in a Russian population.BMC medical genomics · 2019Article
- Yiguanjian decoction enhances fetal liver stem/progenitor cell-mediated repair of liver cirrhosis through regulation of macrophage activation state.World journal of gastroenterology · 2018Article
- The Flavonoid Quercetin Ameliorates Liver Inflammation and Fibrosis by Regulating Hepatic Macrophages Activation and Polarization in Mice.Frontiers in pharmacology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The liver maintains an immunologically tolerant environment as a result of continuous exposure to food and bacterial constituents from the digestive tract. Hepatotropic pathogens can take advantage of this niche and establish lifelong chronic infections causing hepatic fibrosis and hepatocellular carcinoma. Macrophages (Mϕ) play a critical role in regulation of immune responses to hepatic infection and regeneration of tissue. However, the factors crucial for Mϕ in limiting hepatic inflammation or resolving liver damage have not been fully understood. In this report, we demonstrate that expression of C-type lectin receptor scavenger receptor-AI (SR-AI) is crucial for promoting M2-like Mϕ activation and polarization during hepatic inflammation. Liver Mϕ uniquely up-regulated SR-AI during hepatotropic viral infection and displayed increased expression of alternative Mϕ activation markers, such as YM-1, arginase-1, and interleukin-10 by activation of mer receptor tyrosine kinase associated with inhibition of mammalian target of rapamycin. Expression of these molecules was reduced on Mϕ obtained from livers of infected mice deficient for the gene encoding SR-AI (msr1). Furthermore, in vitro studies using an SR-AI-deficient Mϕ cell line revealed impeded M2 polarization and decreased phagocytic capacity. Direct stimulation with virus was sufficient to activate M2 gene expression in the wild-type (WT) cell line, but not in the knockdown cell line. Importantly, tissue damage and fibrosis were exacerbated in SR-AI
conclusionSR-AI expression on liver Mϕ promotes recovery from infection-induced tissue damage by mediating a switch to a proresolving Mϕ polarization state. (Hepatology 2017;65:32-43).
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.