ReviewFrontiers in genetics2015
Mononuclear cells and vascular repair in HHT.
Review in Frontiers in genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Updates on the Pathogenesis and Therapeutic Approaches for Hereditary Hemorrhagic Telangiectasia.Current vascular pharmacology · 2025Review
- Increasing Endoglin Deletion in Endothelial Cells Exacerbates the Severity of Brain Arteriovenous Malformation in Mouse.Biomedicines · 2024Article
- The Role and Therapeutic Implications of Inflammation in the Pathogenesis of Brain Arteriovenous Malformations.Biomedicines · 2023Review
- Prevalence of Intracranial Aneurysms in Hereditary Hemorrhagic Telangiectasia: Report from a Single Reference Center.AJNR. American journal of neuroradiology · 2022Article
- Identification of Key Determinants of Cerebral Malaria Development and Inhibition Pathways.mBio · 2022Article
- A Rare Case of Upper Gastrointestinal Bleeding: Osler-Weber-Rendu Syndrome.Medicina (Kaunas, Lithuania) · 2022Article
- An update on preclinical models of hereditary haemorrhagic telangiectasia: Insights into disease mechanisms.Frontiers in medicine · 2022Review
- Pilot investigation of circulating angiogenic and inflammatory biomarkers associated with vascular malformations.Orphanet journal of rare diseases · 2021Article
- Bone marrow mononuclear cells for joint therapy: The role of macrophages in inflammation resolution and tissue repair.World journal of stem cells · 2021Review
- Review
- Pulmonary Vascular Complications in Hereditary Hemorrhagic Telangiectasia and the Underlying Pathophysiology.International journal of molecular sciences · 2021Review
- Transcriptional and Histochemical Signatures of Bone Marrow Mononuclear Cell-Mediated Resolution of Synovitis.Frontiers in immunology · 2021Article
- Endoglin: Beyond the Endothelium.Biomolecules · 2020Review
- Reduction of endoglin receptor impairs mononuclear cell-migration.Exploration of medicine · 2020Article
- Decreased levels of miR-28-5p and miR-361-3p and increased levels of insulin-like growth factor 1 mRNA in mononuclear cells from patients with hereditary hemorrhagic telangiectasiaCanadian journal of physiology and pharmacology · 2019Article
- Soluble endoglin regulates expression of angiogenesis-related proteins and induction of arteriovenous malformations in a mouse model of hereditary hemorrhagic telangiectasia.Disease models & mechanisms · 2018Article
- Bone Morphogenetic Proteins in Vascular Homeostasis and Disease.Cold Spring Harbor perspectives in biology · 2018Review
- The roles of endoglin gene in cerebrovascular diseases.Neuroimmunology and neuroinflammation · 2017Article
- Persistent infiltration and pro-inflammatory differentiation of monocytes cause unresolved inflammation in brain arteriovenous malformation.Angiogenesis · 2016Article
- Regulatory RNAs controlling vascular (dys)function by affecting TGF-ß family signalling.EXCLI journal · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hereditary hemorrhagic telangiectasia (HHT) or Rendu-Osler-Weber disease is a rare genetic vascular disorder known for its endothelial dysplasia causing arteriovenous malformations and severe bleedings. HHT-1 and HHT-2 are the most prevalent variants and are caused by heterozygous mutations in endoglin and activin receptor-like kinase 1, respectively. An undervalued aspect of the disease is that HHT patients experience persistent inflammation. Although endothelial and mural cells have been the main research focus trying to unravel the mechanism behind the disease, wound healing is a process with a delicate balance between inflammatory and vascular cells. Inflammatory cells are part of the mononuclear cells (MNCs) fraction, and can, next to eliciting an immune response, also have angiogenic potential. This biphasic effect of MNC can hold a promising mechanism to further elucidate treatment strategies for HHT patients. Before MNC are able to contribute to repair, they need to home to and retain in ischemic and damaged tissue. Directed migration (homing) of MNCs following tissue damage is regulated by the stromal cell derived factor 1 (SDF1). MNCs that express the C-X-C chemokine receptor 4 (CXCR4) migrate toward the tightly regulated gradient of SDF1. This directed migration of monocytes and lymphocytes can be inhibited by dipeptidyl peptidase 4 (DPP4). Interestingly, MNC of HHT patients express elevated levels of DPP4 and show impaired homing toward damaged tissue. Impaired homing capacity of the MNCs might therefore contribute to the impaired angiogenesis and tissue repair observed in HHT patients. This review summarizes recent studies regarding the role of MNCs in the etiology of HHT and vascular repair, and evaluates the efficacy of DPP4 inhibition in tissue integrity and repair.
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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.