ArticleAging2020
AKT3 deficiency in M2 macrophages impairs cutaneous wound healing by disrupting tissue remodeling.
Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Cholesterol efflux protein, ABCA1, supports anticancer functions of myeloid immune cells.Science advances · 2026Article
- Loss of Akt3 enhances antiviral immunity while disrupting corneal homeostasis during ocular HSV-1 infection.Frontiers in immunology · 2026Article
- Mild and reversible nephrotoxicity following repeated administration of damnacanthal in nude mice.Toxicology reports · 2025Article
- Article
- Computational Insights into the Polypharmacological Landscape of BCR-ABL Inhibitors: Emphasis on Imatinib and Nilotinib.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Elevation of Plasma IL-15 and RANTES as Potential Biomarkers of Healing in Chronic Venous Ulcerations: A Pilot Study.Biomolecules · 2025Article
- LncRNA UCA1 regulates immune micro-environment in cisplatin-induced AKI by miRNA-4498/AKT3 pathway.PloS one · 2025Article
- AXL-TBK1 driven AKT3 activation promotes metastasis.Science signaling · 2024Article
- M2 macrophages promote subconjunctival fibrosis through YAP/TAZ signalling.Annals of medicine · 2024Article
- Analysis of subsets and localization of macrophages in skin lesions and peripheral blood of patients with keloids.Heliyon · 2024Article
- LLLT accelerates experimental wound healing under microgravity conditions via PI3K/AKT-CCR2 signal axis.Frontiers in bioengineering and biotechnology · 2024Article
- Advances in the study of macrophage polarization in inflammatory immune skin diseases.Journal of inflammation (London, England) · 2023Review
- [LRG1 inhibits hepatic macrophage activation by enhancing TGF-β1 signaling to alleviate MAFLD in mice].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Extended characterization of IL-33/ST2 as a predictor for wound age determination in skin wound tissue samples of humans and mice.International journal of legal medicine · 2023Article
- SENP3 deletion promotes M2 macrophage polarization and accelerates wound healing through smad6/IκB/p65 signaling pathway.Heliyon · 2023Article
- The regulation mechanism of different hair types in inner Mongolia cashmere goat based on PI3K-AKT pathway and FGF21.Journal of animal science · 2022Article
- Lactate metabolism in human health and disease.Signal transduction and targeted therapy · 2022Review
- Akt isoforms in the immune system.Frontiers in immunology · 2022Review
- Article
- miR-150 and SRPK1 regulate AKT3 expression to participate in LPS-induced inflammatory response.Innate immunity · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AKT signaling and M2 macrophage-guided tissue repair are key factors in cutaneous wound healing. A delay in this process threatens human health worldwide. However, the role of AKT3 in delayed cutaneous wound healing is largely unknown. In this study, histological staining and transcriptomics demonstrated that prolonged tissue remodeling delayed wound healing. This delay was accompanied by defects in AKT3, collagen alpha-1(I) chain (COL1A1), and collagen alpha-1(XI) chain (COL11A1) expression and AKT signaling. The defect in AKT3 expression was M2 macrophage-specific, and decreased AKT3 protein levels were observed in CD68/CD206-positive macrophages from delayed wound tissue. Downregulation of AKT3 in M2 macrophages did not influence cell polarization but impaired collagen organization by inhibiting COL1A1 and COL11A1 expression in human skin fibroblasts (HSFs). Moreover, a co-culture model revealed that the downregulation of AKT3 in the human monocytic cell line (THP-1)-derived M2 macrophages impaired HSF proliferation and migration. Finally, cutaneous wound healing in AKT3
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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.