ArticleThe Journal of clinical investigation2005
Akt1/protein kinase Balpha is critical for ischemic and VEGF-mediated angiogenesis.
Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 220 papers, 1 of them a synthesis that pooled it.
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Who cites it
220 citing papers in PubMed, 1 synthesis or guideline pooled it, 385 citations in OpenAlex.
- Macrophage-associated kinase signaling in atherosclerosis - a systematic review.Cell communication and signaling : CCS · 2026Pooled it
- Human iPSC-EV-loaded nanofiber stent coatings accelerate vascular repair by enhancing EGFR/HIF-1α signaling and suppressing ROCK1-mediated remodeling.Materials today. Bio · 2026Article
- Endothelial cell-specific DNA methylation alterations in breast cancer.Communications biology · 2026Article
- Integrative molecular simulations reveal NeuroAid II mechanisms in ischemic stroke through network pharmacology, molecular dynamics, and pharmacophore modeling.Scientific reports · 2026Article
- Role of Matricellular Proteins in Endothelial Cell Inflammation and Atherosclerosis.Antioxidants (Basel, Switzerland) · 2025Review
- Semaphorin 3F is elevated in serum of heart failure patients and inhibits cardiac angiogenesis via the VEGF/Akt/eNOS pathway.Journal of molecular and cellular cardiology plus · 2025Article
- Deficiency in N-cadherin-Akt3 signaling impairs the blood-brain barrier.Cell reports · 2025Article
- Vascular endothelial growth factor signaling in health and disease: from molecular mechanisms to therapeutic perspectives.Signal transduction and targeted therapy · 2025Review
- Long noncoding RNA VPS9D1-AS1 promotes angiogenesis in colorectal cancer by regulating the VEGFA signalling pathway.American journal of cancer research · 2025Article
- Vulnerable plaques in atherosclerosis: focus on angiogenesis-associated phenotypic crosstalk.Frontiers in pharmacology · 2025Review
- Unveiling the Role of Mechanistic Target of Rapamycin Kinase (MTOR) Signaling in Cancer Progression and the Emergence of MTOR Inhibitors as Therapeutic Strategies.ACS pharmacology & translational science · 2024Review
- Mechanism of Artemisia annua L. in the treatment of acute myocardial infarction: network pharmacology, molecular docking and in vivo validation.Molecular diversity · 2024Article
- Akt is a mediator of artery specification during zebrafish development.Development (Cambridge, England) · 2024Article
- CCL11 released by GSDMD-mediated macrophage pyroptosis regulates angiogenesis after hindlimb ischemia.Cell death discovery · 2024Article
- Muscone abrogates breast cancer progression through tumor angiogenic suppression via VEGF/PI3K/Akt/MAPK signaling pathways.Cancer cell international · 2024Article
- Increase in Vascular Endothelial Growth Factor (VEGF) Expression and the Pathogenesis of iMCD-TAFRO.Biomedicines · 2024Review
- Akt3 activation by R-Ras in an endothelial cell enforces quiescence and barrier stability of neighboring endothelial cells via Jagged1.Cell reports · 2024Article
- Cysteine-rich with EGF-like domains 2 (CRELD2) is an endoplasmic reticulum stress-inducible angiogenic growth factor promoting ischemic heart repair.Nature cardiovascular research · 2024Article
- Investigation of the Potential Mechanism of Compound Dragon's Blood Capsule against Myocardial Ischemia Based on Network Pharmacology.Combinatorial chemistry & high throughput screening · 2024Article
- Loss of Histone Methyltransferase KMT2D Attenuates Angiogenesis in the Ischemic Heart by Inhibiting the Transcriptional Activation of VEGF-A.Journal of cardiovascular translational research · 2023Article
160 more citing papers are in PubMed but not listed here.
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12 authors at 1 institution in 1 country.
Funding
Abstract
Akt, or protein kinase B, is a multifunctional serine-threonine protein kinase implicated in a diverse range of cellular functions including cell metabolism, survival, migration, and gene expression. However, the in vivo roles and effectors of individual Akt isoforms in signaling are not explicitly clear. Here we show that the genetic loss of Akt1, but not Akt2, in mice results in defective ischemia and VEGF-induced angiogenesis as well as severe peripheral vascular disease. Akt1 knockout (Akt1-/-) mice also have reduced endothelial progenitor cell (EPC) mobilization in response to ischemia, and reintroduction of WT EPCs, but not EPCs isolated from Akt1-/- mice, into WT mice improves limb blood flow after ischemia. Mechanistically, the loss of Akt1 reduces the basal phosphorylation of several Akt substrates, the migration of fibroblasts and ECs, and NO release. Reconstitution of Akt1-/- ECs with Akt1 rescues the defects in substrate phosphorylation, cell migration, and NO release. Thus, the Akt1 isoform exerts an essential role in blood flow control, cellular migration, and NO synthesis during postnatal angiogenesis.
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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.