ArticleHaematologica2023
APOLD1 loss causes endothelial dysfunction involving cell junctions, cytoskeletal architecture, and Weibel-Palade bodies, while disrupting hemostasis.
Article in Haematologica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 30 citations in OpenAlex.
- FAIMS-GPF XL-MS: crosslinking-mass spectrometry based on gas-phase fractionation.Nature communications · 2026Article
- Restoring RCAN1 dosage mitigates sleep and EEG abnormalities in a Down syndrome model.Neurobiology of disease · 2026Article
- Abnormal whole-blood viscoelastic test results in patients with bleeding disorder of unknown cause.Blood vessels, thrombosis & hemostasis · 2026Article
- Identification of Paraptosis-Related Renal Cell Carcinoma Subtypes, Construction of a Prognostic Signature, and Determination of Tumor Microenvironment Landscape Using Bioinformatic Analysis and Experimental Verification.Current issues in molecular biology · 2026Article
- Distinct transcriptional and epigenomic programs define Hofbauer cells in term placenta.JCI insight · 2026Article
- Silicate biomaterials-based multicellular scaffolds with specific cellular spatial distribution for infarcted myocardium repair.Bioactive materials · 2026Article
- COL1A2 and APOLD1 Define a Dual-Axis Molecular Framework for Diabetic Nephropathy-Retinopathy Comorbidity: An Integrative Multiomics and Machine Learning Study in Mouse Models.International journal of medical sciences · 2026Article
- Lineage-Biased Neural Stem Cell Grafting Promotes Neuronal Differentiation and Vascular Repair in the Chronic Phase of Stroke.CNS neuroscience & therapeutics · 2026Article
- RadiotherapyTranslational lung cancer research · 2025Article
- Single nucleus RNA sequencing unveils relationship between microglia and endothelial cells in mixed Alzheimer's disease and vascular pathology.Neurobiology of disease · 2025Article
- Impact of Alzheimer's disease risk factors and local neuromelanin content on the transcriptomic landscape of the human locus coeruleus.bioRxiv : the preprint server for biology · 2025Article
- Ischaemic preconditioning regulates cardiac transcriptome via DNA methylation conferring cardio-protection from ischaemic reperfusion injury.European heart journal open · 2025Article
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- Versatile effects of galectin-1 protein-containing lipid bilayer coating for cardiovascular applications.Bioactive materials · 2024Article
- LRG1 loss effectively restrains glomerular TGF-β signaling to attenuate diabetic kidney disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Clinical and genetic associations of asymmetric apical and septal left ventricular hypertrophy.European heart journal. Digital health · 2024Article
- Prognostic and predictive value of super-enhancer-derived signatures for survival and lung metastasis in osteosarcoma.Journal of translational medicine · 2024Article
- The 330 risk loci known for systemic lupus erythematosus (SLE): a review.Frontiers in lupus · 2024Article
- The vascular gene Apold1 is dispensable for normal development but controls angiogenesis under pathological conditions.Angiogenesis · 2023Article
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Authors and funding
10 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular homeostasis is impaired in various diseases thereby contributing to the progression of their underlying pathologies. The endothelial immediate early gene Apolipoprotein L domain-containing 1 (APOLD1) helps to regulate endothelial function. However, its precise role in endothelial cell biology remains unclear. We have localized APOLD1 to endothelial cell contacts and to Weibel-Palade bodies (WPB) where it associates with von Willebrand factor (VWF) tubules. Silencing of APOLD1 in primary human endothelial cells disrupted the cell junction-cytoskeletal interface, thereby altering endothelial permeability accompanied by spontaneous release of WPB contents. This resulted in an increased presence of WPB cargoes, notably VWF and angiopoietin-2 in the extracellular medium. Autophagy flux, previously recognized as an essential mechanism for the regulated release of WPB, was impaired in the absence of APOLD1. In addition, we report APOLD1 as a candidate gene for a novel inherited bleeding disorder across three generations of a large family in which an atypical bleeding diathesis was associated with episodic impaired microcirculation. A dominant heterozygous nonsense APOLD1:p.R49* variant segregated to affected family members. Compromised vascular integrity resulting from an excess of plasma angiopoietin-2, and locally impaired availability of VWF may explain the unusual clinical profile of APOLD1:p.R49* patients. In summary, our findings identify APOLD1 as an important regulator of vascular homeostasis and raise the need to consider testing of endothelial cell function in patients with inherited bleeding disorders without apparent platelet or coagulation defects.
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