ArticleNature cardiovascular research2025
Angiopoietin-TIE2 feedforward circuit promotes PIK3CA-driven venous malformations.
Abstract read
In one paragraph
Article in Nature cardiovascular research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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
18 citing papers in PubMed.
- Clinical and molecular characterization of non-PIK3CA-related vascular malformations with overgrowth in a pediatric cohort.World journal of pediatrics : WJP · 2026Article
- From Somatic Driver to Molecular Therapy in Retinal, Choroidal and Periocular Vascular Disease: Mosaicism, Targetable Pathways and Ocular Toxicity.International journal of molecular sciences · 2026Review
- Review
- A high-sensitivity TIE2-GRB2 BRET platform for functional and pharmacologic profiling of pathogenic variants associated with venous malformations.Angiogenesis · 2026Article
- Endocardial TIE2 orchestrates cardiac trabeculation via sequestering FOXO1 within the cytoplasm and stimulating versican cleavage.Development (Cambridge, England) · 2026Article
- Inactive β1-integrin acts as a junctional scaffold for angiopoietin/TIE2/FOXO1 signaling.The Journal of clinical investigation · 2026Article
- TIE2 links MEKK3-KLF2/4 and PI3K signaling in cerebral cavernous malformation.The Journal of experimental medicine · 2026Article
- A human endothelial and adipose stem cell-based co-culture model for venous malformations.Angiogenesis · 2026Article
- Trp53 loss drives the neoplastic transformation of Pik3caH1047R-induced vascular malformation in a mouse model.PloS one · 2026Article
- ANGPT1-GABARAP axis modulates NLRP3 inflammasome-mediated pyroptosis in Crohn's disease.Frontiers in immunology · 2026Article
- Vascular malformations: from genetics to therapeutics.EMBO molecular medicine · 2026Review
- Advances in genetics, signaling, and modeling of venous malformations.Frontiers in cardiovascular medicine · 2026Review
- Identification of pathological CD133+ endothelial cells in venous malformations.Frontiers in cardiovascular medicine · 2026Article
- PI3K/AKT/mTOR axis in vascular malformations: from molecular insights to targeted clinical trials.Orphanet journal of rare diseases · 2025Review
- Recurrent somatic copy number alterations in resected cerebral cavernous malformations.Human genomics · 2025Article
- Association between angiopoietin-1 and metabolic dysfunction-associated steatotic liver disease: a cross‑sectional study.Diabetology & metabolic syndrome · 2025Article
- From Mutation to Prognosis: AI-HOPE-PI3K Enables Artificial Intelligence Agent-Driven Integration of PI3K Pathway Data in Colorectal Cancer Precision Medicine.International journal of molecular sciences · 2025Article
- Serum VEGF and ANGPT1 as angiogenesis markers may predict the outcomes of older adults with hip fractures.Frontiers in medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Marle KraftUppsala University, Department of Immunology, Genetics and Pathology, Uppsala, Sweden.ORCID http://orcid.org/0000-0002-3523-7003
Hans Schoofs *Uppsala University, Department of Immunology, Genetics and Pathology, Uppsala, Sweden.ORCID http://orcid.org/0000-0003-3429-912X
Milena Petkova *Uppsala University, Department of Immunology, Genetics and Pathology, Uppsala, Sweden.ORCID http://orcid.org/0000-0002-7186-7256
Jorge AndradeAngiogenesis & Metabolism Laboratory, Center of Vascular Biomedicine, Berlin Institute of Health at Charité - Universitätsmedizin Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0002-4577-8620
Ana Rita GrossoAssociate Laboratory i4HB - Institute for Health and Bioeconomy, NOVA School of Science and Technology, Universidade NOVA de Lisboa, Lisbon, Portugal.ORCID http://orcid.org/0000-0001-6974-4209
Rui BeneditoMolecular Genetics of Angiogenesis Group. Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.ORCID http://orcid.org/0000-0003-2458-3055
An-Katrien De RooCenter for Vascular Anomalies, VASCERN VASCA European Reference Center, Cliniques Universitaires Saint Luc, UCLouvain, Brussels, Belgium.ORCID http://orcid.org/0000-0002-0000-1260
Laurence M BoonCenter for Vascular Anomalies, VASCERN VASCA European Reference Center, Cliniques Universitaires Saint Luc, UCLouvain, Brussels, Belgium.ORCID http://orcid.org/0000-0001-8273-3328
Miikka VikkulaCenter for Vascular Anomalies, VASCERN VASCA European Reference Center, Cliniques Universitaires Saint Luc, UCLouvain, Brussels, Belgium.ORCID http://orcid.org/0000-0002-6236-338X
Friedrich G KappDepartment of Pediatric Hematology and Oncology, Children's Hospital, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, VASCERN VASCA European Reference Center, Freiburg, Germany.ORCID http://orcid.org/0000-0002-2729-6177
René HägerlingResearch Group 'Lymphovascular Medicine and Translational 3D-Histopathology', Institute of Medical and Human Genetics, Charité-Universitätsmedizin Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0002-6830-2043
Michael PotenteAngiogenesis & Metabolism Laboratory, Center of Vascular Biomedicine, Berlin Institute of Health at Charité - Universitätsmedizin Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0002-5689-0036
Taija MäkinenUppsala University, Department of Immunology, Genetics and Pathology, Uppsala, Sweden. taija.makinen@igp.uu.se.ORCID http://orcid.org/0000-0002-9338-1257
Funding
Cancerfonden (Swedish Cancer Society) 19 0220 Pj, 22 2025 PjEC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) 101078827EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) 773047EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 Marie Sklodowska-Curie Actions (H2020 Excellent Science - Marie Sklodowska-Curie Actions) 814316Fonds De La Recherche Scientifique - FNRS (Belgian National Fund for Scientific Research) T.00.19.22 and P.C013.20Fonds De La Recherche Scientifique - FNRS (Belgian National Fund for Scientific Research) T.0240.23 & P.C005.22Knut och Alice Wallenbergs Stiftelse (Knut and Alice Wallenberg Foundation) 2018.0218Knut och Alice Wallenbergs Stiftelse (Knut and Alice Wallenberg Foundation) 2020.0057Sigrid Juséliuksen Säätiö (Sigrid Jusélius Foundation) 240137Vetenskapsrådet (Swedish Research Council) 2020-0269
Abstract
Venous malformations (VMs) are vascular anomalies lacking curative treatments, often caused by somatic PIK3CA mutations that hyperactivate the PI3Kα-AKT-mTOR signaling pathway. Here, we identify a venous-specific signaling circuit driving disease progression, where excessive PI3Kα activity amplifies upstream TIE2 receptor signaling through autocrine and paracrine mechanisms. In Pik3ca
Indexed as
Angiopoietin-1Angiopoietin-2Class I Phosphatidylinositol 3-KinasesEndothelial CellsReceptor, TIE-2Vascular MalformationsVeinsAnimalsDisease Models, AnimalForkhead Box Protein O1HumansMiceMutationMyocytes, Smooth MusclePhenotypeProto-Oncogene Proteins c-aktAngiopoietin-1Angiopoietin-2ANGPT1 protein, humanAngpt1 protein, mouseANGPT2 protein, humanAngpt2 protein, mouseClass I Phosphatidylinositol 3-KinasesForkhead Box Protein O1FOXO1 protein, humanFoxo1 protein, mouseMTOR protein, humanmTOR protein, mousePIK3CA protein, humanPik3ca protein, mouseProto-Oncogene Proteins c-aktReceptor, TIE-2TEK protein, humanTek protein, mouseTOR Serine-Threonine Kinases
Identifiers
What Socratic holds
Textmetadata
LicenceCC BY
Read underepoch 390
Registered trials
None linked
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 Socratic graph.