Human blood vessel organoids as a model of diabetic vasculopathy
Open accessAbstract
The increasing prevalence of diabetes has resulted in a global epidemic 1. Diabetes is a major cause of blindness, kidney failure, heart attacks, stroke and amputation of lower limbs. These are often caused by changes in blood vessels, such as the expansion of the basement membrane and a loss of vascular cells 2-4. Diabetes also impairs the functions of endothelial cells 5 and disturbs the communication between endothelial cells and pericytes 6. How dysfunction of endothelial cells and/or pericytes leads to diabetic vasculopathy remains largely unknown. Here we report the development of self-organizing three-dimensional human blood vessel organoids from pluripotent stem cells. These human blood vessel organoids contain endothelial cells and pericytes that self-assemble into capillary networks that are enveloped by a basement membrane. Human blood vessel organoids transplanted into mice form a stable, perfused vascular tree, including arteries, arterioles and venules. Exposure of blood vessel organoids to hyperglycaemia and inflammatory cytokines in vitro induces thickening of the vascular basement membrane. Human blood vessels, exposed in vivo to a diabetic milieu in mice, also mimic the microvascular changes found in patients with diabetes. DLL4 and NOTCH3 were identified as key drivers of diabetic vasculopathy in human blood vessels. Therefore, organoids derived from human stem cells faithfully recapitulate the structure and function of human blood vessels and are amenable systems for modelling and identifying the regulators of diabetic vasculopathy, a disease that affects hundreds of millions of patients worldwide.
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The pathological microenvironment in diabetic bone defect areas is characterized by hyperglycemia, chronic inflammation, vascular dysfunction, and immune dysregulation.
“The pathological microenvironment in DM bone defect areas is characterized by hyperglycemia, chronic inflammation, vascular dysfunction, and immune dysregulation4–6.”
From Microenvironment-responsive multifunctional enzyme-linked hydrogel for diabetic bone defect regeneration. (2025) · cites this paper as [4]
The paper’s Abstract describes hyperglycemia, an inflammatory state involving TNFα and IL6, and vascular abnormalities in diabetes; it also reports basement-membrane changes in diabetic vascular organoids and patients’ dermal microvessels. It does not establish that this combination characterizes diabetic bone-defect areas, or address immune dysregulation there. (LLM, conf=0.88)
Experimental — accuracy not yet measuredhiPSC-derived blood vessel organoids yield self-assembled endothelial networks with lumina and mural support cells capable of forming perfusable vascular structures.
“In parallel, advances in the generation of hiPSCderived blood vessel organoids (BVOs) have yielded selfassembled endothelial networks with lumina and mural support cells capable of forming perfusable vascular structures.”
From Vascularized human skin assembloids model compartmental skin organization and immune responsiveness in vitro (2026) · cites this paper as [17]
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- Authors
- Wimmer, R. A., Leopoldi, A., Aichinger, M., Wick, N., Hantusch, B., Novatchkova, M., Taubenschmid, J., Hämmerle, M., Esk, C., Bagley, J. A., Lindenhofer, D., Chen, G., Boehm, M., Agu, C. A., Yang, F., Fu, B., Zuber, J., Knoblich, J. A., Kerjaschki, D., & Penninger, J. M.
- Affiliations
- Institute of Molecular Biotechnology (AT)
- Research Institute of Molecular Pathology (AT)
- Medical University of Vienna (AT)
- National Institutes of Health (US)
- Wellcome Sanger Institute (GB)
- Corresponding author
- Wimmer, Reiner A.
- Penninger, Josef M.
- ORCID
- Wimmer, Reiner A.
- Leopoldi, Alexandra
- Aichinger, Martin
- Wick, Nikolaus
- Hantusch, Brigitte
- Novatchkova, Maria
- Taubenschmid, Jasmin
- Esk, Christopher
- Bagley, Joshua A.
- Lindenhofer, Dominik
- Chen, Guibin
- Boehm, Manfred
- Agu, Chukwuma A.
- Yang, Fengtang
- Fu, Beiyuan
- Zuber, Johannes
- Knoblich, Juergen A.
- Kerjaschki, Dontscho
- Penninger, Josef M.
- Venue
- Nature
- Published
- 2019-01
- Volume
- 565
- Issue
- 7740
- Pages
- 505-510
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC7116578
- OpenAlex
- W2908930063
- Cited by
- 803
- References
- 45
- Citations by year
- 2026: 100 · 2025: 116 · 2024: 112 · 2023: 109 · 2022: 111 · 2021: 113 · 2020: 79 · 2019: 62
- FWCI
- 30.52
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Nature
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Keywords
- diabetic vascular disease, blood vessel organoids, pluripotent stem cells, endothelial cells, pericytes, basement membrane thickening, hyperglycemia, inflammatory cytokines, DLL4, Notch3, capillary network, organoid transplantation, microvascular dysfunction, disease modeling
- MeSH terms
- Receptor, Notch3, Animals, Arteries, Arterioles, Basement Membrane, Blood Vessels, Calcium-Binding Proteins, Diabetic Angiopathies, Humans, Hyperglycemia, Models, Biological, Organoids, Venules, Signal Transduction, Inflammation Mediators, Pericytes, Intercellular Signaling Peptides and Proteins, Pluripotent Stem Cells, Endothelial Cells, Adaptor Proteins, Signal Transducing, Mice, Amyloid Precursor Protein Secretases, In Vitro Techniques
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Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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