ArticleFrontiers in pharmacology2024
Danlian-Tongmai formula improves diabetic vascular calcification by regulating CCN3/NOTCH signal axis to inhibit inflammatory reaction.
Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Proteomic Risk Score for Prediction of Incident Hypertension.Hypertension (Dallas, Tex. : 1979) · 2026Article
- Integrating Chinese medicine and intermittent fasting: A promising approach for treating diabetic vascular calcification.Acta pharmaceutica Sinica. B · 2026Article
- Chinese medicine and intermittent fasting integration therapy attenuate diabetic vascular calcificationActa pharmaceutica Sinica. B · 2026Article
- Isowighteone attenuates vascular calcification by targeting HSP90AA1-mediated PI3K-Akt pathway and suppressing osteogenic gene expression.Frontiers in bioengineering and biotechnology · 2025Article
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7 authors.
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Abstract
Background: Vascular calcification (VC) commonly occurs in diabetes and is associated with cardiovascular disease incidence and mortality. Currently, there is no drug treatment for VC. The Danlian-Tongmai formula (DLTM) is a traditional Chinese medicine (TCM) prescription used for diabetic VC (DVC), but its mechanisms of action remain unclear. This study aims to elucidate the effects of DLTM on DVC and explore the underlying mechanisms of action. Methods: Ultra-high-performance liquid chromatography-mass spectrometry (UHPLC-MS) was used to identify the metabolites of DLTM. A DVC rat model was established using streptozotocin (STZ) combined with vitamin D3 (VitD3). The effects of DLTM on DVC were evaluated through alizarin red staining, calcium deposition, and changes in osteogenic and contractile markers. The specific molecular mechanism of DLTM in treating diabetic VC was comprehensively analyzed by transcriptomics, molecular docking and Results: We identified 108 major metabolites of DLTM. Conclusion: DLTM alleviates DVC by regulating the CCN3/NOTCH signaling axis to inhibit inflammatory responses. Our research provides experimental basis for clinical treatment and drug transformation of diabetic VC.
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