ArticleNature communications2017
Uncontrolled angiogenic precursor expansion causes coronary artery anomalies in mice lacking Pofut1.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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
26 citing papers in PubMed, 41 citations in OpenAlex.
- TM4SF1 mediates YAP/TAZ regulation of coronary artery formation.Scientific reports · 2026Article
- Molecular Framework of the Onset and Progression of Skeletal Muscle Aging.International journal of molecular sciences · 2025Review
- Atrial Fibroblasts-Derived Extracellular Vesicles Exacerbate Atrial Arrhythmogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Congenital Coronary Blood Vessel Anomalies: Animal Models and the Integration of Developmental Mechanisms.Advances in experimental medicine and biology · 2024Article
- EOGT enables residual Notch signaling in mouse intestinal cells lacking POFUT1.Scientific reports · 2023Article
- Preliminary study on the mechanism of POFUT1 in colorectal cancer.Medical oncology (Northwood, London, England) · 2023Article
- Prerequisite endocardial-mesenchymal transition for murine cardiac trabecular angiogenesis.Developmental cell · 2023Article
- Synergistic regulation of Notch signaling by different O-glycans promotes hematopoiesis.Frontiers in immunology · 2023Article
- Identification of 5 hub genes for diagnosis of coronary artery disease.Frontiers in cardiovascular medicine · 2023Article
- Cryo-EM structures of human fucosidase FucA1 reveal insight into substrate recognition and catalysis.Structure (London, England : 1993) · 2022Article
- A SOX17-PDGFB signaling axis regulates aortic root development.Nature communications · 2022Article
- Notch signaling pathway: architecture, disease, and therapeutics.Signal transduction and targeted therapy · 2022Review
- Two genetic variants inFrontiers in cardiovascular medicine · 2022Article
- Perinatal angiogenesis from pre-existing coronary vessels via DLL4-NOTCH1 signalling.Nature cell biology · 2021Article
- Endothelial sprouting, proliferation, or senescence: tipping the balance from physiology to pathology.Cellular and molecular life sciences : CMLS · 2021Review
- Multifaceted regulation of Notch signaling by glycosylation.Glycobiology · 2021Review
- Other Types of Glycosylation.Advances in experimental medicine and biology · 2021Article
- Control of sinus venous valve and sinoatrial node development by endocardial NOTCH1.Cardiovascular research · 2020Article
- POFUT1 is dispensable for structure, function and survival of mouse podocytes.American journal of translational research · 2020Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 5 institutions in 5 countries.
Funding
Abstract
Coronary artery anomalies may cause life-threatening cardiac complications; however, developmental mechanisms underpinning coronary artery formation remain ill-defined. Here we identify an angiogenic cell population for coronary artery formation in mice. Regulated by a DLL4/NOTCH1/VEGFA/VEGFR2 signaling axis, these angiogenic cells generate mature coronary arteries. The NOTCH modulator POFUT1 critically regulates this signaling axis. POFUT1 inactivation disrupts signaling events and results in excessive angiogenic cell proliferation and plexus formation, leading to anomalous coronary arteries, myocardial infarction and heart failure. Simultaneous VEGFR2 inactivation fully rescues these defects. These findings show that dysregulated angiogenic precursors link coronary anomalies to ischemic heart disease.Though coronary arteries are crucial for heart function, the mechanisms guiding their formation are largely unknown. Here, Wang et al. identify a unique, endocardially-derived angiogenic precursor cell population for coronary artery formation in mice and show that a DLL4/NOTCH1/VEGFA/VEGFR2 signaling axis is key for coronary artery development.
Indexed as
Identifiers
What OpenQuestion holds
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.