ArticleArteriosclerosis, thrombosis, and vascular biology2018
Endothelial Cell Autonomous Role of Akt1: Regulation of Vascular Tone and Ischemia-Induced Arteriogenesis.
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Article in Arteriosclerosis, thrombosis, and vascular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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27citing papers in PubMed, 1 pooled it
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
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- Finerenone Alleviates Cardiac Microvascular Injury and Neutrophil Extracellular Traps Formation in Diabetic Cardiomyopathy via Regulating AKT1 Phosphorylation.Acta physiologica (Oxford, England) · 2026Article
- Endothelial Nucleoporin93 (Nup93) Maintains Vascular Homeostasis via Sun1-Dependent Regulation of RhoA/ROCK Activity.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Endothelial cell-specific DNA methylation alterations in breast cancer.Communications biology · 2026Article
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- Single-cell profiling reveals transcriptomic signatures of vascular endothelial cells in non-healing diabetic foot ulcers.Frontiers in endocrinology · 2023Article
- Activation of the aryl hydrocarbon receptor by clozapine induces preadipocyte differentiation and contributes to endothelial dysfunction.Journal of psychopharmacology (Oxford, England) · 2022Article
- Type 2 Diabetes Complicated With Heart Failure: Research on Therapeutic Mechanism and Potential Drug Development Based on Insulin Signaling Pathway.Frontiers in pharmacology · 2022Review
- Protein kinase N2 mediates flow-induced endothelial NOS activation and vascular tone regulation.The Journal of clinical investigation · 2021Article
- Paracrine interleukin-8 affects mesenchymal stem cells through the Akt pathway and enhances human umbilical vein endothelial cell proliferation and migration.Bioscience reports · 2021Article
- Aerobic Exercise Restores Aging-Associated Reductions in Arterial Adropin Levels and Improves Adropin-Induced Nitric Oxide-Dependent Vasorelaxation.Journal of the American Heart Association · 2021Article
- Network pharmacology and molecular docking study on the active ingredients of qidengmingmu capsule for the treatment of diabetic retinopathy.Scientific reports · 2021Article
- The subcellular redistribution of NLRC5 promotes angiogenesis via interacting with STAT3 in endothelial cells.Theranostics · 2021Article
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Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Monica Y LeeFrom the Vascular Biology and Therapeutics Program, Department of Pharmacology (M.Y.L., A.G.-M., J.K., W.C.S.), Vascular Biology and Therapeutics Program, Department of Pathology (T.R.K.), and Department of Cell Biology (M.S.), Yale University School of Medicine, New Haven, CT; Department of Internal Medicine, Section of Cardiovascular Medicine, Yale Cardiovascular Research Center, New Haven, CT (J.Z., Z.Z., M.S.); Department of Chemistry, Yale University, New Haven, CT (D.J.V., G.W.B.); and Department of Internal Medicine, VA Connecticut Healthcare System, West Haven, CT (H.V.).
Ana Gamez-MendezFrom the Vascular Biology and Therapeutics Program, Department of Pharmacology (M.Y.L., A.G.-M., J.K., W.C.S.), Vascular Biology and Therapeutics Program, Department of Pathology (T.R.K.), and Department of Cell Biology (M.S.), Yale University School of Medicine, New Haven, CT; Department of Internal Medicine, Section of Cardiovascular Medicine, Yale Cardiovascular Research Center, New Haven, CT (J.Z., Z.Z., M.S.); Department of Chemistry, Yale University, New Haven, CT (D.J.V., G.W.B.); and Department of Internal Medicine, VA Connecticut Healthcare System, West Haven, CT (H.V.).
Jiasheng ZhangFrom the Vascular Biology and Therapeutics Program, Department of Pharmacology (M.Y.L., A.G.-M., J.K., W.C.S.), Vascular Biology and Therapeutics Program, Department of Pathology (T.R.K.), and Department of Cell Biology (M.S.), Yale University School of Medicine, New Haven, CT; Department of Internal Medicine, Section of Cardiovascular Medicine, Yale Cardiovascular Research Center, New Haven, CT (J.Z., Z.Z., M.S.); Department of Chemistry, Yale University, New Haven, CT (D.J.V., G.W.B.); and Department of Internal Medicine, VA Connecticut Healthcare System, West Haven, CT (H.V.).
Zhenwu ZhuangFrom the Vascular Biology and Therapeutics Program, Department of Pharmacology (M.Y.L., A.G.-M., J.K., W.C.S.), Vascular Biology and Therapeutics Program, Department of Pathology (T.R.K.), and Department of Cell Biology (M.S.), Yale University School of Medicine, New Haven, CT; Department of Internal Medicine, Section of Cardiovascular Medicine, Yale Cardiovascular Research Center, New Haven, CT (J.Z., Z.Z., M.S.); Department of Chemistry, Yale University, New Haven, CT (D.J.V., G.W.B.); and Department of Internal Medicine, VA Connecticut Healthcare System, West Haven, CT (H.V.).
David J VinyardFrom the Vascular Biology and Therapeutics Program, Department of Pharmacology (M.Y.L., A.G.-M., J.K., W.C.S.), Vascular Biology and Therapeutics Program, Department of Pathology (T.R.K.), and Department of Cell Biology (M.S.), Yale University School of Medicine, New Haven, CT; Department of Internal Medicine, Section of Cardiovascular Medicine, Yale Cardiovascular Research Center, New Haven, CT (J.Z., Z.Z., M.S.); Department of Chemistry, Yale University, New Haven, CT (D.J.V., G.W.B.); and Department of Internal Medicine, VA Connecticut Healthcare System, West Haven, CT (H.V.).
Jan KraehlingFrom the Vascular Biology and Therapeutics Program, Department of Pharmacology (M.Y.L., A.G.-M., J.K., W.C.S.), Vascular Biology and Therapeutics Program, Department of Pathology (T.R.K.), and Department of Cell Biology (M.S.), Yale University School of Medicine, New Haven, CT; Department of Internal Medicine, Section of Cardiovascular Medicine, Yale Cardiovascular Research Center, New Haven, CT (J.Z., Z.Z., M.S.); Department of Chemistry, Yale University, New Haven, CT (D.J.V., G.W.B.); and Department of Internal Medicine, VA Connecticut Healthcare System, West Haven, CT (H.V.).
Heino VelazquezFrom the Vascular Biology and Therapeutics Program, Department of Pharmacology (M.Y.L., A.G.-M., J.K., W.C.S.), Vascular Biology and Therapeutics Program, Department of Pathology (T.R.K.), and Department of Cell Biology (M.S.), Yale University School of Medicine, New Haven, CT; Department of Internal Medicine, Section of Cardiovascular Medicine, Yale Cardiovascular Research Center, New Haven, CT (J.Z., Z.Z., M.S.); Department of Chemistry, Yale University, New Haven, CT (D.J.V., G.W.B.); and Department of Internal Medicine, VA Connecticut Healthcare System, West Haven, CT (H.V.).
Gary W BrudvigFrom the Vascular Biology and Therapeutics Program, Department of Pharmacology (M.Y.L., A.G.-M., J.K., W.C.S.), Vascular Biology and Therapeutics Program, Department of Pathology (T.R.K.), and Department of Cell Biology (M.S.), Yale University School of Medicine, New Haven, CT; Department of Internal Medicine, Section of Cardiovascular Medicine, Yale Cardiovascular Research Center, New Haven, CT (J.Z., Z.Z., M.S.); Department of Chemistry, Yale University, New Haven, CT (D.J.V., G.W.B.); and Department of Internal Medicine, VA Connecticut Healthcare System, West Haven, CT (H.V.).
Themis R KyriakidesFrom the Vascular Biology and Therapeutics Program, Department of Pharmacology (M.Y.L., A.G.-M., J.K., W.C.S.), Vascular Biology and Therapeutics Program, Department of Pathology (T.R.K.), and Department of Cell Biology (M.S.), Yale University School of Medicine, New Haven, CT; Department of Internal Medicine, Section of Cardiovascular Medicine, Yale Cardiovascular Research Center, New Haven, CT (J.Z., Z.Z., M.S.); Department of Chemistry, Yale University, New Haven, CT (D.J.V., G.W.B.); and Department of Internal Medicine, VA Connecticut Healthcare System, West Haven, CT (H.V.).
Michael SimonsFrom the Vascular Biology and Therapeutics Program, Department of Pharmacology (M.Y.L., A.G.-M., J.K., W.C.S.), Vascular Biology and Therapeutics Program, Department of Pathology (T.R.K.), and Department of Cell Biology (M.S.), Yale University School of Medicine, New Haven, CT; Department of Internal Medicine, Section of Cardiovascular Medicine, Yale Cardiovascular Research Center, New Haven, CT (J.Z., Z.Z., M.S.); Department of Chemistry, Yale University, New Haven, CT (D.J.V., G.W.B.); and Department of Internal Medicine, VA Connecticut Healthcare System, West Haven, CT (H.V.).
William C SessaFrom the Vascular Biology and Therapeutics Program, Department of Pharmacology (M.Y.L., A.G.-M., J.K., W.C.S.), Vascular Biology and Therapeutics Program, Department of Pathology (T.R.K.), and Department of Cell Biology (M.S.), Yale University School of Medicine, New Haven, CT; Department of Internal Medicine, Section of Cardiovascular Medicine, Yale Cardiovascular Research Center, New Haven, CT (J.Z., Z.Z., M.S.); Department of Chemistry, Yale University, New Haven, CT (D.J.V., G.W.B.); and Department of Internal Medicine, VA Connecticut Healthcare System, West Haven, CT (H.V.). william.sessa@yale.edu.
Yale University · USVA Connecticut Healthcare System · US
Funding
SOCS-1 and endothelial dysfunction in graft arteriosclerosisP01HL070295 · NHLBI · YALE UNIVERSITY · PI TELLIDES, GEORGE · 2001 to 2010
$17.9MRenal Physiology and Phenotyping CoreP30DK079310 · NIDDK · YALE UNIVERSITY · PI SOMLO, STEFAN · 2008 to 2022
$16.8MAngiogensis and ischemiaR01HL053793 · NHLBI · YALE UNIVERSITY · PI SIMONS, MICHAEL · 1996 to 2017
$7.3MPHOSPHORYLATION AND ENDOTHELIAL NITRIC OXIDE PRODUCTIONR01HL064793 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2000 to 2016
$6.3MMCP-1 and attenuation of the foreign body responseR01GM072194 · NIGMS · YALE UNIVERSITY · PI KYRIAKIDES, THEMIS R · 2005 to 2018
$4.7MInsights into the Molecular and Cellular Mechanisms governing Endothelial FunctionR35HL139945 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2018 to 2021
$4.3MRegulation of vascular remodeling &angiogenesis by NogoR01HL081190 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2005 to 2014
$4.1MEndothelial NOS by Protein-Protein IntractionsR01HL061371 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 1999 to 2008
$3.6MAkt-mediated regulation of endothelial functionsK99HL130581 · NHLBI · YALE UNIVERSITY · PI LEE, MONICA Y · 2016 to 2017
$212kAn isoform-specific, conditional deletion approach to decipher Akt1 and Akt2 funcF32HL119147 · NHLBI · YALE UNIVERSITY · PI LEE, MONICA Y · 2013 to 2015
$159kNHLBI NIH HHS F32 HL119147NHLBI NIH HHS K99 HL130581NHLBI NIH HHS P01 HL070295NHLBI NIH HHS R01 HL053793NHLBI NIH HHS R01 HL061371NHLBI NIH HHS R01 HL064793NHLBI NIH HHS R01 HL081190NHLBI NIH HHS R35 HL139945NIDDK NIH HHS P30 DK079310NIGMS NIH HHS R01 GM072194
Abstract
objectiveThe importance of PI3K/Akt signaling in the vasculature has been demonstrated in several models, as global loss of Akt1 results in impaired postnatal ischemia- and VEGF-induced angiogenesis. The ubiquitous expression of Akt1, however, raises the possibility of cell-type-dependent Akt1-driven actions, thereby necessitating tissue-specific characterization. APPROACH AND
resultsHerein, we used an inducible, endothelial-specific Akt1-deleted adult mouse model (Akt1iECKO) to characterize the endothelial cell autonomous functions of Akt1 in the vascular system. Endothelial-targeted ablation of Akt1 reduces eNOS (endothelial nitric oxide synthase) phosphorylation and promotes both increased vascular contractility in isolated vessels and elevated diastolic blood pressures throughout the diurnal cycle in vivo. Furthermore, Akt1iECKO mice subject to the hindlimb ischemia model display impaired blood flow and decreased arteriogenesis.
conclusionsEndothelial Akt1 signaling is necessary for ischemic resolution post-injury and likely reflects the consequence of NO insufficiency critical for vascular repair.
Indexed as
Neovascularization, PhysiologicVasoconstrictionAnimalsAorta, ThoracicBlood Flow VelocityBlood PressureDisease Models, AnimalEndothelial CellsHindlimbIschemiaMaleMice, KnockoutMuscle, SkeletalNitric OxideNitric Oxide Synthase Type IIIPhosphorylationAkt1 protein, mouseNitric OxideNitric Oxide Synthase Type IIINos3 protein, mouseProto-Oncogene Proteins c-aktblood pressureendothelial cellhindlimbhomeostasisphosphorylation
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