ArticlePloS one2014
Myeloid-specific Rictor deletion induces M1 macrophage polarization and potentiates in vivo pro-inflammatory response to lipopolysaccharide.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
What it found
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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.
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Who cites it
61 citing papers in PubMed, 127 citations in OpenAlex.
- Hematopoiesis could be improved by correcting aberrant bone marrow macrophages polarization in aplastic anemia patients.Science China. Life sciences · 2026Article
- Decoding atherosclerosis through lactylation: multi-omics integration with experimental validation.Frontiers in cell and developmental biology · 2026Article
- mTORC2 inhibition reduces tumor burden via STAT1 activation and enhanced response to anti-PD-L1 therapy.Cell death & disease · 2025Article
- Rictor Ameliorates Acute Antibody-Mediated Rejection Following Kidney Transplantation by Suppressing Macrophage M1 Polarization Through p65-NLRP3 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Downregulation of exosomal miR-let-7e-5p induces macrophage M2 polarization by targeting Rictor/AKT1 signal pathway in brucellosis patients.European journal of medical research · 2025Article
- Angiotensin II Type 2 Receptor Inhibits M1 Polarization and Apoptosis of Alveolar Macrophage and Protects Against Mechanical Ventilation-Induced Lung Injury.Inflammation · 2025Article
- Loss of Macrophage mTORC2 Drives Atherosclerosis via FoxO1 and IL-1β Signaling.Circulation research · 2023Article
- Mechanistic/mammalian target of rapamycin complex 1 (mTORC1) signaling is involved in phagocytosis activation during THP-1 cell differentiation.The Journal of veterinary medical science · 2023Article
- Targeting the biology of aging with mTOR inhibitors.Nature aging · 2023Review
- Adipose tissue macrophages as potential targets for obesity and metabolic diseases.Frontiers in immunology · 2023Review
- Article
- Neuropeptide Y Promotes Human M2 Macrophage Polarization and Enhances p62/SQSTM1-Dependent Autophagy and NRF2 Activation.International journal of molecular sciences · 2022Article
- Elp3-mediated codon-dependent translation promotes mTORC2 activation and regulates macrophage polarization.The EMBO journal · 2022Article
- Phenotype Diversity of Macrophages in Osteoarthritis: Implications for Development of Macrophage Modulating Therapies.International journal of molecular sciences · 2022Review
- Modulation of mTOR Signaling in Cardiovascular Disease to Target Acute and Chronic Inflammation.Frontiers in cardiovascular medicine · 2022Review
- AKT Isoforms in Macrophage Activation, Polarization, and Survival.Current topics in microbiology and immunology · 2022Article
- Efferocytosis in multisystem diseases (Review).Molecular medicine reports · 2022Review
- Rosmarinic Acid Regulates Microglial M1/M2 Polarization via the PDPK1/Akt/HIF Pathway Under Conditions of Neuroinflammation.Inflammation · 2021Article
- Roles of Macrophages in the Development and Treatment of Gut Inflammation.Frontiers in cell and developmental biology · 2021Review
- Expanding TOR Complex 2 Signaling: Emerging Regulators and New Connections.Frontiers in cell and developmental biology · 2021Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
Abstract
The phosphoinositide-3-kinase (PI3K)/protein kinase B (Akt) axis plays a central role in attenuating inflammation upon macrophage stimulation with toll-like receptor (TLR) ligands. The mechanistic target of rapamycin complex 2 (mTORC2) relays signal from PI3K to Akt but its role in modulating inflammation in vivo has never been investigated. To evaluate the role of mTORC2 in the regulation of inflammation in vivo, we have generated a mouse model lacking Rictor, an essential mTORC2 component, in myeloid cells. Primary macrophages isolated from myeloid-specific Rictor null mice exhibited an exaggerated response to TLRs ligands, and expressed high levels of M1 genes and lower levels of M2 markers. To determine whether the loss of Rictor similarly affected inflammation in vivo, mice were either fed a high fat diet, a situation promoting chronic but low-grade inflammation, or were injected with lipopolysaccharide (LPS), which mimics an acute, severe septic inflammatory condition. Although high fat feeding contributed to promote obesity, inflammation, macrophage infiltration in adipose tissue and systemic insulin resistance, we did not observe a significant impact of Rictor loss on these parameters. However, mice lacking Rictor exhibited a higher sensitivity to septic shock when injected with LPS. Altogether, these results indicate that mTORC2 is a key negative regulator of macrophages TLR signalling and that its role in modulating inflammation is particularly important in the context of severe inflammatory challenges. These observations suggest that approaches aimed at modulating mTORC2 activity may represent a possible therapeutic approach for diseases linked to excessive inflammation.
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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.