ArticleOncotarget2018
NOD2 deficiency exacerbates hypoxia-induced pulmonary hypertension and enhances pulmonary vascular smooth muscle cell proliferation.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 22 citations in OpenAlex.
- RO4929097 inhibits NICD3 to alleviate pulmonary hypertension via blocking Notch3/HIF-2α/FoxM1 signaling pathway.In vitro cellular & developmental biology. Animal · 2025Article
- RNA-seq analysis of extracellular vesicles from hyperphosphatemia-stimulated endothelial cells provides insight into the mechanism underlying vascular calcification.BMC nephrology · 2022Article
- Inhibition of mitoNEET attenuates LPS-induced inflammation and oxidative stress.Cell death & disease · 2022Article
- Mechanism of Hypoxia-Mediated Smooth Muscle Cell Proliferation Leading to Vascular Remodeling.BioMed research international · 2022Review
- Angiotensin-converting enzyme 2 alleviates pulmonary artery hypertension through inhibition of focal adhesion kinase expression.Experimental and therapeutic medicine · 2021Article
- Inborn Errors in the LRR Domain of Nod2 and Their Potential Consequences on the Function of the Receptor.Cells · 2021Review
- Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of nucleotide-binding oligomerization domain protein 2 (NOD2) is upregulated in pulmonary artery smooth muscle cells (PASMCs) during hypoxia. To investigate the involvement of NOD2 in the pulmonary vascular response to hypoxia, we subjected wild-type and NOD2-deficient mice to chronic normobaric hypoxic conditions. Compared to wild-type mice, NOD2-deficient mice developed severe pulmonary hypertension with exaggerated elevation of right ventricular systolic pressure, profound right ventricular hypertrophy and striking vascular remodeling after exposure to hypoxia. Pulmonary vascular remodeling in NOD2-deficient mice was characterized by increased PASMC proliferation. Furthermore, hypoxia-inducible factor-1α expression and Akt phosphorylation were upregulated in PASMCs from NOD2-deficient mice exposed to hypoxia. Our findings revealed that the absence of NOD2 exacerbated hypoxia-induced PASMC proliferation, pulmonary hypertension and vascular remodeling, but had no effect on PASMC migration or contractility.
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Registered trials
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