ArticleThe Biochemical journal2013
PDGF-mediated autophagy regulates vascular smooth muscle cell phenotype and resistance to oxidative stress.
Article in The Biochemical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.
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Who cites it
120 citing papers in PubMed, 217 citations in OpenAlex.
- Sex-Specific Proteomic Profiling Identifies Pregnancy Zone Protein as a Complement-Linked Marker of Adverse Prognosis in Esophageal Adenocarcinoma.International journal of cancer · 2026Article
- Vascular calcification: pathogenic mechanisms, signaling crosstalk and translational therapeutics.Signal transduction and targeted therapy · 2026Review
- TRIM24 Impediment suppresses VSMC modulation and attenuates neointimal hyperplasia via redox and autophagy pathways.Molecular biology reports · 2026Article
- Exercise Attenuates Aortic Dissection Via PDE5A-Mediated Inhibition of Vascular Smooth Muscle Cell Phenotypic Switch.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Crosstalk between inflammation and autophagy in CeD organoids.Scientific reports · 2026Article
- Distinct types of regulated cell death in atherosclerosis.Journal of pharmaceutical analysis · 2026Review
- Regulation of Periodontal Ligament Autophagy by Super-Activated Platelet Lysate in a Rat Maxillary Expansion Model.Drug design, development and therapy · 2026Article
- Targeting autophagy in dysfunctional tumor vasculature.iScience · 2025Review
- Defective autophagy in vascular smooth muscle cells promote uremic accelerated atherosclerosis.Renal failure · 2025Article
- C-Kit Is Essential for Vascular Smooth Muscle Cell Phenotypic Switch In Vitro and In Vivo After Injury.Cells · 2025Article
- SOX6 enhances vascular smooth muscle cell phenotypic switching and elevates blood pressure by activating autophagy.Animal models and experimental medicine · 2025Article
- Novel roles of Nrf3-Trim5 axis in vascular smooth muscle cell dysfunctions and neointimal hyperplasia.Cardiovascular research · 2025Article
- The crosstalk between non-coding RNAs and oxidative stress in cancer progression.Genes & diseases · 2025Review
- Identification of the CeRNA axis of circ_0000006/miR-483-5p/KDM2B in the progression of aortic aneurysm to aorta dissection.BMC cardiovascular disorders · 2025Article
- Hsa_circ_0001304 promotes vascular neointimal hyperplasia accompanied by autophagy activation.Communications biology · 2025Article
- The multifaceted role of autophagy and mitophagy in cardiovascular health and disease.Autophagy reports · 2025Review
- The potential mechanism of celastrol attenuating atherosclerosis by promoting macrophage autophagy via AMPK/ULK1 pathway.Frontiers in pharmacology · 2025Article
- The Role of Autophagy in Erectile Dysfunction.The world journal of men's health · 2025Review
- Review
- Autophagy as a Guardian of Vascular Niche Homeostasis.International journal of molecular sciences · 2024Review
60 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Vascular injury and chronic arterial diseases result in exposure of VSMCs (vascular smooth muscle cells) to increased concentrations of growth factors. The mechanisms by which growth factors trigger VSMC phenotype transitions remain unclear. Because cellular reprogramming initiated by growth factors requires not only the induction of genes involved in cell proliferation, but also the removal of contractile proteins, we hypothesized that autophagy is an essential modulator of VSMC phenotype. Treatment of VSMCs with PDGF (platelet-derived growth factor)-BB resulted in decreased expression of the contractile phenotype markers calponin and α-smooth muscle actin and up-regulation of the synthetic phenotype markers osteopontin and vimentin. Autophagy, as assessed by LC3 (microtubule-associated protein light chain 3 α; also known as MAP1LC3A)-II abundance, LC3 puncta formation and electron microscopy, was activated by PDGF exposure. Inhibition of autophagy with 3-methyladenine, spautin-1 or bafilomycin stabilized the contractile phenotype. In particular, spautin-1 stabilized α-smooth muscle cell actin and calponin in PDGF-treated cells and prevented actin filament disorganization, diminished production of extracellular matrix, and abrogated VSMC hyperproliferation and migration. Treatment of cells with PDGF prevented protein damage and cell death caused by exposure to the lipid peroxidation product 4-hydroxynonenal. The results of the present study demonstrate a distinct form of autophagy induced by PDGF that is essential for attaining the synthetic phenotype and for survival under the conditions of high oxidative stress found to occur in vascular lesions.
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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.