ArticleBasic research in cardiology2012
Inhibition of STAT3 signaling prevents vascular smooth muscle cell proliferation and neointima formation.
Article in Basic research in cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 60 citations in OpenAlex.
- Vein graft failure: Pathophysiology, detection, prevention and emerging therapeutic strategies.Pharmacological reviews · 2026Review
- TNF-α-Induced Upregulation of ADAMTS-8 Expression in SW480 Cells: Implications for Intracellular Signaling Pathways and Transcription Factor Activity.Cell biochemistry and biophysics · 2026Article
- Adventitial Fibroblasts Release Interleukin 6 After Vascular Injury and Induce Smooth Muscle Cell Proliferation and Neointima Formation.Journal of the American Heart Association · 2025Article
- Proline-driven metabolic reprogramming promotes skeletal muscle hypertrophy and oxidative myofiber specification in porcine offspring: a stage-optimized maternal nutritional intervention.Journal of animal science and biotechnology · 2025Article
- SOX9 mediates the phenotypic transformation of vascular smooth muscle cells in restenosis after carotid artery injury.Frontiers in cell and developmental biology · 2025Article
- STAT protein family and cardiovascular diseases: overview of pathological mechanisms and therapeutic implications.Molecular biology reports · 2024Review
- Signaling through the IL-6-STAT3 Pathway Promotes Proteolytically-Active Macrophage Accumulation Necessary for Development of Small AAA.Vascular and endovascular surgery · 2023Article
- Gene-repressing epigenetic reader EED unexpectedly enhances cyclinD1 gene activation.Molecular therapy. Nucleic acids · 2023Article
- Transcription factors: key regulatory targets of vascular smooth muscle cell in atherosclerosis.Molecular medicine (Cambridge, Mass.) · 2023Review
- Matrix protein Tenascin-C promotes kidney fibrosis via STAT3 activation in response to tubular injury.Cell death & disease · 2022Article
- Extracellular traps from activated vascular smooth muscle cells drive the progression of atherosclerosis.Nature communications · 2022Article
- DR1 Activation Inhibits the Proliferation of Vascular Smooth Muscle Cells through Increasing Endogenous HAging and disease · 2022Article
- Deletion of Smooth Muscle Lethal Giant Larvae 1 Promotes Neointimal Hyperplasia in Mice.Frontiers in pharmacology · 2022Article
- Shexiang Baoxin Pills Inhibited Proliferation and Migration of Human Coronary Artery Smooth Muscle CellsFrontiers in cardiovascular medicine · 2021Article
- JANEX-1 improves acute pulmonary embolism through VEGF and FAK in pulmonary artery smooth muscle cells.Experimental biology and medicine (Maywood, N.J.) · 2020Article
- Article
- Semaphorin-3A protects against neointimal hyperplasia after vascular injury.EBioMedicine · 2019Article
- Therapeutic Targeting of the Proinflammatory IL-6-JAK/STAT Signalling Pathways Responsible for Vascular Restenosis in Type 2 Diabetes Mellitus.Cardiology research and practice · 2019Review
- Targeted inhibition of STAT3 as a potential treatment strategy for atherosclerosis.Theranostics · 2019Review
- Transforming growth factor β1 suppresses proinflammatory gene program independent of its regulation on vascular smooth muscle differentiation and autophagy.Cellular signalling · 2018Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dedifferentiation, migration, and proliferation of resident vascular smooth muscle cells (SMCs) are key components of neointima formation after vascular injury. Activation of signal transducer and activator of transcription-3 (STAT3) is suggested to be critically involved in this process, but the complex regulation of STAT3-dependent genes and the functional significance of inhibiting this pathway during the development of vascular proliferative diseases remain elusive. In this study, we demonstrate that STAT3 was activated in neointimal lesions following wire-induced injury in mice. Phosphorylation of STAT3 induced trans-activation of cyclin D1 and survivin in SMCs in vitro and in neointimal cells in vivo, thus promoting proliferation and migration of SMCs as well as reducing apoptotic cell death. WP1066, a highly potent inhibitor of STAT3 signaling, abrogated phosphorylation of STAT3 and dose-dependently inhibited the functional effects of activated STAT3 in stimulated SMCs. The local application of WP1066 via a thermosensitive pluronic F-127 gel around the dilated arteries significantly inhibited proliferation of neointimal cells and decreased the neointimal lesion size at 3 weeks after injury. Even though WP1066 application attenuated the injury-induced up-regulation of the chemokine RANTES at 6 h after injury, there was no significant effect on the accumulation of circulating cells at 1 week after injury. In conclusion, these data identify STAT3 as a key molecule for the proliferative response of SMC and neointima formation. Moreover, inhibition of STAT3 by the potent and specific compound WP1066 might represent a novel and attractive approach for the local treatment of vascular proliferative diseases.
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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.