ArticleNutrients2023
Molecular Mechanism of Calycosin Inhibited Vascular Calcification.
Article in Nutrients, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Targeting Vascular Calcification: Novel Insights into Molecular Pathways and Clinical Interventions.Cardiovascular drugs and therapy · 2026Review
- Pharmacological modulation of Ca²⁺ signaling by calycosin promotes glioblastoma cell death.Medical oncology (Northwood, London, England) · 2026Article
- Emerging Role of Calycosin in Inflammatory Diseases: Molecular Mechanisms and Potential Therapeutic Applications.Biomolecules · 2025Review
- Ershen Dan attenuates atherosclerosis by modulating the NOTCH1/NF-κB/NLRP3 signaling pathway to suppress M1 macrophage polarization.Chinese medicine · 2025Article
- Beyond Traditional Use: The Scientific Evidence for the Role ofPharmaceuticals (Basel, Switzerland) · 2025Review
- From Traditional Efficacy to Drug Design: A Review of Astragali Radix.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Calycosin suppresses the activating effect of granulocyte-macrophage-colony-stimulating factor-producing T helper cells on macrophages in experimental atherosclerosis.Frontiers in pharmacology · 2025Article
- The Role of NOTCH Pathway Genes in the Inherited Susceptibility to Aortic Stenosis.Journal of cardiovascular development and disease · 2024Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Vascular calcification (VC) is a pathological condition frequently observed in cardiovascular diseases. Primary factors contributing to VC are osteogenic differentiation of vascular smooth muscle and hydroxyapatite deposition. Targeted autophagy (a lysosome-mediated mechanism for degradation/recycling of unnecessary cellular components) is a useful approach for inhibiting VC and promoting vascular cell health. Calycosin has been shown to alleviate atherosclerosis by enhancing macrophage autophagy, but its therapeutic effect on VC has not been demonstrated. Using an in vitro model (rat thoracic aortic smooth muscle cell line A7r5), we demonstrated effective inhibition of VC using calycosin (the primary flavonoid component of astragalus), based on the enhancement of autophagic flux. Calycosin treatment activated AMPK/mTOR signaling to induce initiation of autophagy and restored mTORC1-dependent autophagosome-lysosome fusion in late-stage autophagy by promoting soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex formation, thereby preventing stoppage of autophagy in calcified cells. Calycosin substantially reduced degrees of both osteogenic differentiation and calcium deposition in our VC cell model by enhancing autophagy. The present findings clarify the mechanism whereby calycosin mitigates autophagy stoppage in calcified smooth muscle cells and provide a basis for effective VC treatment via autophagy enhancement.
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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.