ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015
Hematopoietic Akt2 deficiency attenuates the progression of atherosclerosis.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- The role of natural products targeting macrophage polarization in sepsis-induced lung injury.Chinese medicine · 2025Review
- Trained immunity in atherosclerosis: plasticity, metabolic-vascular axis, and AI-driven precision remodeling.Frontiers in immunology · 2025Review
- Aberrant mitochondrial DNA synthesis in macrophages exacerbates inflammation and atherosclerosis.Nature communications · 2024Article
- Article
- Macrophage-Derived 25-Hydroxycholesterol Promotes Vascular Inflammation, Atherogenesis, and Lesion Remodeling.Circulation · 2023Article
- Endothelial nitric oxide synthase (eNOS) S1176 phosphorylation status governs atherosclerotic lesion formation.Frontiers in cardiovascular medicine · 2023Article
- Liver macrophages and inflammation in physiology and physiopathology of non-alcoholic fatty liver disease.The FEBS journal · 2022Review
- MK2206 attenuates atherosclerosis by inhibiting lipid accumulation, cell migration, proliferation, and inflammation.Acta pharmacologica Sinica · 2022Article
- Posttranscriptional Regulation of Insulin Resistance: Implications for Metabolic Diseases.Biomolecules · 2022Review
- AKT2 deficiency impairs formation of the BCR signalosome.Cell communication and signaling : CCS · 2020Article
- The Anti-atherogenic Role of Exercise Is Associated With the Attenuation of Bone Marrow-Derived Macrophage Activation and Migration in Hypercholesterolemic Mice.Frontiers in physiology · 2020Article
- Akt Signaling in Macrophage Polarization, Survival, and Atherosclerosis.International journal of molecular sciences · 2019Review
- Loss of 2 Akt (Protein Kinase B) Isoforms in Hematopoietic Cells Diminished Monocyte and Macrophage Survival and Reduces Atherosclerosis in Ldl Receptor-Null Mice.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- M2 Macrophages as a Potential Target for Antiatherosclerosis Treatment.Neural plasticity · 2019Review
- The Akt pathway in oncology therapy and beyond (Review).International journal of oncology · 2018Review
- DHEA inhibits acute microglia-mediated inflammation through activation of the TrkA-Akt1/2-CREB-Jmjd3 pathway.Molecular psychiatry · 2018Article
- Integrin beta3 regulates clonality and fate of smooth muscle-derived atherosclerotic plaque cells.Nature communications · 2018Article
- microRNA-612 is downregulated by platelet-derived growth factor-BB treatment and has inhibitory effects on vascular smooth muscle cell proliferation and migration via directly targeting AKT2.Experimental and therapeutic medicine · 2018Article
- Opposing Actions of AKT (Protein Kinase B) Isoforms in Vascular Smooth Muscle Injury and Therapeutic Response.Arteriosclerosis, thrombosis, and vascular biology · 2017Article
- Macrophage deficiency of miR-21 promotes apoptosis, plaque necrosis, and vascular inflammation during atherogenesis.EMBO molecular medicine · 2017Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Atherosclerosis is the major cause of death and disability in diabetic and obese subjects with insulin resistance. Akt2, a phosphoinositide-dependent serine-threonine protein kinase, is highly express in insulin-responsive tissues; however, its role during the progression of atherosclerosis remains unknown. Thus, we aimed to investigate the contribution of Akt2 during the progression of atherosclerosis. We found that germ-line Akt2-deficient mice develop similar atherosclerotic plaques as wild-type mice despite higher plasma lipids and glucose levels. It is noteworthy that transplantation of bone marrow cells isolated from Akt2(-/-) mice to Ldlr(-/-) mice results in marked reduction of the progression of atherosclerosis compared with Ldlr(-/-) mice transplanted with wild-type bone marrow cells. In vitro studies indicate that Akt2 is required for macrophage migration in response to proatherogenic cytokines (monocyte chemotactic protein-1 and macrophage colony-stimulating factor). Moreover, Akt2(-/-) macrophages accumulate less cholesterol and have an alternative activated or M2-type phenotype when stimulated with proinflammatory cytokines. Together, these results provide evidence that macrophage Akt2 regulates migration, the inflammatory response and cholesterol metabolism and suggest that targeting Akt2 in macrophages might be beneficial for treating atherosclerosis.
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Registered trials
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