ArticleJournal of lipid research2014
Macrophage deficiency of Akt2 reduces atherosclerosis in Ldlr null mice.
Article in Journal of lipid research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 63 citations in OpenAlex.
- The miR-125a-5p/IRF4 Axis Mediates Sodium Arsenite-Induced M2 Macrophage Polarization.Biomolecules · 2025Article
- The role of natural products targeting macrophage polarization in sepsis-induced lung injury.Chinese medicine · 2025Review
- Potential mechanistic linkages of Naoluotong granules on the remission of atherosclerosis by multidimensional analysis.Heliyon · 2024Article
- Differential effects of AKT1 and AKT2 on sleep-wake activity under basal conditions and in response to LPS challenge in mice.Sleep and biological rhythms · 2024Article
- Role of macrophage polarization in heart failure and traditional Chinese medicine treatment.Frontiers in pharmacology · 2024Review
- Review
- Macrophage polarization states in atherosclerosis.Frontiers in immunology · 2023Review
- MicroRNA and Hemostasis Profile of Carotid Atherosclerosis.International journal of molecular sciences · 2022Article
- MK2206 attenuates atherosclerosis by inhibiting lipid accumulation, cell migration, proliferation, and inflammation.Acta pharmacologica Sinica · 2022Article
- Protein Kinase B2 (PKB2/AKT2) Is Essential for Host Protection in CVB3-Induced Acute Viral Myocarditis.International journal of molecular sciences · 2022Article
- AKT Isoforms in Macrophage Activation, Polarization, and Survival.Current topics in microbiology and immunology · 2022Article
- Metabolic Regulation of Macrophage Activation.Journal of innate immunity · 2022Review
- PI3K regulates the activation of NLRP3 inflammasome in atherosclerosis through part-dependent AKT signaling pathway.Experimental animals · 2021Article
- Roles of Macrophages in Atherogenesis.Frontiers in pharmacology · 2021Review
- Macrophage Paired Immunoglobulin-Like Receptor B Deficiency Promotes Peripheral Atherosclerosis in Apolipoprotein E-Deficient Mice.Frontiers in cell and developmental biology · 2021Article
- Macrophage Plasticity and Atherosclerosis Therapy.Frontiers in molecular biosciences · 2021Review
- Anti-Inflammatory Activity of Extracts and Pure Compounds Derived from Plants via Modulation of Signaling Pathways, Especially PI3K/AKT in Macrophages.International journal of molecular sciences · 2020Review
- AKT2 deficiency impairs formation of the BCR signalosome.Cell communication and signaling : CCS · 2020Article
- Macrophages in Atherosclerosis Regression.Arteriosclerosis, thrombosis, and vascular biology · 2020Review
- THP-1 macrophage cholesterol efflux is impaired by palmitoleate through Akt activation.PloS one · 2020Article
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 1 country.
Funding
Abstract
Macrophages play crucial roles in the formation of atherosclerotic lesions. Akt, a serine/threonine protein kinase B, is vital for cell proliferation, migration, and survival. Macrophages express three Akt isoforms, Akt1, Akt2, and Akt3, but the roles of Akt1 and Akt2 in atherosclerosis in vivo remain unclear. To dissect the impact of macrophage Akt1 and Akt2 on early atherosclerosis, we generated mice with hematopoietic deficiency of Akt1 or Akt2. After 8 weeks on Western diet, Ldlr(-/-) mice reconstituted with Akt1(-/-) fetal liver cells (Akt1(-/-)→Ldlr(-/-)) had similar atherosclerotic lesion areas compared with control mice transplanted with WT cells (WT→Ldlr(-/-)). In contrast, Akt2(-/-)→Ldlr(-/-) mice had dramatically reduced atherosclerotic lesions compared with WT→Ldlr(-/-) mice of both genders. Similarly, in the setting of advanced atherosclerotic lesions, Akt2(-/-)→Ldlr(-/-) mice had smaller aortic lesions compared with WT→Ldlr(-/-) and Akt1(-/-)→Ldlr(-/-) mice. Importantly, Akt2(-/-)→Ldlr(-/-) mice had reduced numbers of proinflammatory blood monocytes expressing Ly-6C(hi) and chemokine C-C motif receptor 2. Peritoneal macrophages isolated from Akt2(-/-) mice were skewed toward an M2 phenotype and showed decreased expression of proinflammatory genes and reduced cell migration. Our data demonstrate that loss of Akt2 suppresses the ability of macrophages to undergo M1 polarization reducing both early and advanced atherosclerosis.
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.