ArticleInternational journal of biological sciences2021
Celastrol ameliorates vascular neointimal hyperplasia through Wnt5a-involved autophagy.
Article in International journal of biological sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 35 citations in OpenAlex.
- Fusobacterium nucleatum promotes senescence of human oral mucosa fibroblasts via the Wnt5A/mTOR pathway.Odontology · 2026Article
- Celastrol ameliorates atherosclerosis by inhibiting TLR4/STAT3/NLRP3-mediated macrophage pyroptosis.Chinese medicine · 2026Article
- Mechanistic Insights and Therapeutic Potential of Wnt5a Signaling in Alveolar Epithelial Cell Development and Bronchopulmonary Dysplasia.Stem cell reviews and reports · 2025Review
- Recombinant high-density lipoprotein targeted delivery of celastrol to promote foam cells lipophagy against early atherosclerosis.Journal of nanobiotechnology · 2025Article
- Hsa_circ_0001304 promotes vascular neointimal hyperplasia accompanied by autophagy activation.Communications biology · 2025Article
- From Physicochemical Constraints to Clinical Prospects of Celastrol: Challenges and Nano Delivery Strategies.International journal of nanomedicine · 2025Review
- Mitochondrial Dysfunction in Cardiac Disease: The Fort Fell.Biomolecules · 2024Review
- Wnt5a-mediated autophagy contributes to the epithelial-mesenchymal transition of human bronchial epithelial cells during asthma.Molecular medicine (Cambridge, Mass.) · 2024Article
- Hsa_circ_0001402 alleviates vascular neointimal hyperplasia through a miR-183-5p-dependent regulation of vascular smooth muscle cell proliferation, migration, and autophagy.Journal of advanced research · 2024Article
- Calcitonin Inhibits Phenotypic Switching of Aortic Smooth Muscle Cells and Neointimal Hyperplasia through the AMP-Activated Protein Kinase/Mechanistic Target of Rapamycin Pathway.ACS pharmacology & translational science · 2024Article
- Autophagy in the pharmacological activities of celastrol (Review).Experimental and therapeutic medicine · 2023Review
- Targeting OPA1-Mediated Mitochondrial Fusion Contributed to Celastrol's Anti-Tumor Angiogenesis Effect.Pharmaceutics · 2022Article
- Celastrol Induces Apoptosis and Autophagy via the AKT/mTOR Signaling Pathway in the Pituitary ACTH-secreting Adenoma Cells.Current medical science · 2022Article
- Celastrol inhibits laser-induced choroidal neovascularization by decreasing VEGF induced proliferation and migration.International journal of ophthalmology · 2022Article
- Endoplasmic Reticulum-Mitochondria Contacts: A Potential Therapy Target for Cardiovascular Remodeling-Associated Diseases.Frontiers in cell and developmental biology · 2021Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neointimal hyperplasia caused by the excessive proliferation of vascular smooth muscle cells (VSMCs) is the pathological basis of restenosis. However, there are few effective strategies to prevent restenosis. Celastrol, a pentacyclic triterpene, has been recently documented to be beneficial to certain cardiovascular diseases. Based on its significant effect on autophagy, we proposed that celastrol could attenuate restenosis through enhancing autophagy of VSMCs. In the present study, we found that celastrol effectively inhibited the intimal hyperplasia and hyperproliferation of VSMCs by inducing autophagy. It was revealed that autophagy promoted by celastrol could induce the lysosomal degradation of c-MYC, which might be a possible mechanism contributing to the reduction of VSMCs proliferation. The Wnt5a/PKC/mTOR signaling pathway was found to be an underlying mechanism for celastrol to induce autophagy and inhibit the VSMCs proliferation. These observations indicate that celastrol may be a novel drug with a great potential to prevent restenosis.
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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.