ArticleThe American journal of pathology2009
Vascular endothelial growth factors C and D induces proliferation of lymphangioleiomyomatosis cells through autocrine crosstalk with endothelium.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Diagnostic performance of VEGF-D for lymphangioleiomyomatosis: a meta-analysis.Jornal brasileiro de pneumologia : publicacao oficial da Sociedade Brasileira de Pneumologia e Tisilogia · 2022Pooled it
- Trial
- Modulation of infiltrating CD206The European respiratory journal · 2025Article
- Iron metabolism disorder and artesunate inhibiting tumor growth by inducing ferroptosis in Lymphangioleiomyomatosis.Respiratory research · 2025Article
- Exploring the Role of Matrix Metalloproteinases as Biomarkers in Sporadic Lymphangioleiomyomatosis and Tuberous Sclerosis Complex. A Pilot Study.Frontiers in medicine · 2021Article
- Clinical-Pathological Conference Series from the Medical University of Graz : Case No 170: A 33-year-old psychologist with severe dyspnea and right-sided chylothorax.Wiener klinische Wochenschrift · 2021Article
- VEGFD Protects Retinal Ganglion Cells and, consequently, Capillaries against Excitotoxic Injury.Molecular therapy. Methods & clinical development · 2020Article
- Angiotensin-converting enzyme inhibitors may affect pulmonary function in lymphangioleiomyomatosis.JCI insight · 2019Article
- Article
- The Lymphangioleiomyomatosis Lung Cell and Its Human Cell Models.American journal of respiratory cell and molecular biology · 2018Review
- Aberrant SYK Kinase Signaling Is Essential for Tumorigenesis Induced by TSC2 Inactivation.Cancer research · 2017Article
- Pharmacological targeting of VEGFR signaling with axitinib inhibits Tsc2-null lesion growth in the mouse model of lymphangioleiomyomatosis.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Review
- Sirolimus, a promising treatment for refractory Kaposiform hemangioendothelioma.Journal of cancer research and clinical oncology · 2014Article
- Lymphatic endothelial differentiation in pulmonary lymphangioleiomyomatosis cells.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2013Article
- Lymphatics in lymphangioleiomyomatosis and idiopathic pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2012Review
- Telocytes are the common cell of origin of both PEComas and GISTs: an evidence-supported hypothesis.Journal of cellular and molecular medicine · 2011Article
- Current views on the function of the lymphatic vasculature in health and disease.Genes & development · 2010Review
- Article
- Lymphangioleiomyoma cells and lymphatic endothelial cells: expression of VEGFR-3 in lymphangioleiomyoma cell clusters.The American journal of pathology · 2010Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lymphangioleiomyomatosis (LAM) is a potentially fatal lung disease characterized by nodules of proliferative smooth muscle-like cells. The exact nature of these LAM cells and their proliferative stimuli are poorly characterized. Herein we report the novel findings that the lymphangiogenic vascular endothelial growth factors (VEGF) C and D induce LAM cell proliferation through activation of their cognate receptor VEGF-R3 and activation of the signaling intermediates Akt/mTOR/S6. Furthermore, we identify expression of the proteoglycan NG2, a marker of immature smooth muscle cells, as a characteristic of LAM cells both in vitro and in human lung tissue. VEGF-C-induced LAM cell proliferation was in part a result of autocrine stimulation that resulted from cross talk with lymphatic endothelial cells. Ultimately, these findings identify the lymphangiogenic VEGF proteins as pathogenic growth factors in LAM disease and at the same time provide a novel pharmacotherapeutic target for a lung disease that to date has no known effective treatment.
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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.