ArticleMolecular biology of the cell2011
NOX4 mediates activation of FoxO3a and matrix metalloproteinase-2 expression by urotensin-II.
Article in Molecular biology of the cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 55 citations in OpenAlex.
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- Oxidative stress in asthma pathogenesis: mechanistic insights and implications for airway smooth muscle dysfunction.Cell and tissue research · 2025Review
- USP25 ameliorates vascular remodeling by deubiquitinating FOXO3 and promoting autophagic degradation of FOXO3.Acta pharmaceutica Sinica. B · 2025Article
- Article
- COL4A3 Mutation Induced Podocyte Apoptosis by Dysregulation of NADPH Oxidase 4 and MMP-2.Kidney international reports · 2023Article
- Urotensin II can Induce Skeletal Muscle Atrophy Associated with Upregulating Ubiquitin-Proteasome System and Inhibiting the Differentiation of Satellite Cells in CRF Mice.Calcified tissue international · 2023Article
- Molecular Mechanisms in Genetic Aortopathy-Signaling Pathways and Potential Interventions.International journal of molecular sciences · 2023Review
- The network map of urotensin-II mediated signaling pathway in physiological and pathological conditions.Journal of cell communication and signaling · 2022Article
- Anti-Inflammatory Effects of Rhamnetin on Bradykinin-Induced Matrix Metalloproteinase-9 Expression and Cell Migration in Rat Brain Astrocytes.International journal of molecular sciences · 2022Article
- Salidroside and isorhamnetin attenuate urotensin II-induced inflammatory responseOncology letters · 2021Article
- Poldip2 mediates blood-brain barrier disruption and cerebral edema by inducing AQP4 polarity loss in mouse bacterial meningitis model.CNS neuroscience & therapeutics · 2020Article
- FOXO transcription factor family in cancer and metastasis.Cancer metastasis reviews · 2020Review
- Update onCancers · 2020Review
- Early Programming of Adult Systemic Essential Hypertension.International journal of molecular sciences · 2020Review
- Regulation of Smooth Muscle Cell Proliferation by NADPH Oxidases in Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2019Review
- p47phox-Dependent Reactive Oxygen Species Stimulate Nuclear Translocation of the FoxO1 Transcription Factor During Metabolic Inhibition in Cardiomyoblasts.Cell biochemistry and biophysics · 2018Article
- Increasing autophagy does not affect neurogenic muscle atrophy.European journal of translational myology · 2018Article
- FOXO3a (Forkhead Transcription Factor O Subfamily Member 3a) Links Vascular Smooth Muscle Cell Apoptosis, Matrix Breakdown, Atherosclerosis, and Vascular Remodeling Through a Novel Pathway Involving MMP13 (Matrix Metalloproteinase 13).Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- The epigenetic landscape related to reactive oxygen species formation in the cardiovascular system.British journal of pharmacology · 2017Review
- The G Protein-Coupled Receptor UT of the Neuropeptide Urotensin II Displays Structural and Functional Chemokine Features.Frontiers in endocrinology · 2017Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The vasoactive peptide urotensin-II (U-II) has been associated with vascular remodeling in different cardiovascular disorders. Although U-II can induce reactive oxygen species (ROS) by the NADPH oxidase NOX4 and stimulate smooth muscle cell (SMC) proliferation, the precise mechanisms linking U-II to vascular remodeling processes remain unclear. Forkhead Box O (FoxO) transcription factors have been associated with redox signaling and control of proliferation and apoptosis. We thus hypothesized that FoxOs are involved in the SMC response toward U-II and NOX4. We found that U-II and NOX4 stimulated FoxO activity and identified matrix metalloproteinase-2 (MMP2) as target gene of FoxO3a. FoxO3a activation by U-II was preceded by NOX4-dependent phosphorylation of c-Jun NH(2)-terminal kinase and 14-3-3 and decreased interaction of FoxO3a with its inhibitor 14-3-3, allowing MMP2 transcription. Functional studies in FoxO3a-depleted SMCs and in FoxO3a(-/-) mice showed that FoxO3a was important for basal and U-II-stimulated proliferation and vascular outgrowth, whereas treatment with an MMP2 inhibitor blocked these responses. Our study identified U-II and NOX4 as new activators of FoxO3a, and MMP2 as a novel target gene of FoxO3a, and showed that activation of FoxO3a by this pathway promotes vascular growth. FoxO3a may thus contribute to progression of cardiovascular diseases associated with vascular remodeling.
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