BGP-15 Inhibits Hyperglycemia-Aggravated VSMC Calcification Induced by High Phosphate

Nagy, Annamária; Pethő, Dávid; Gesztelyi, Rudolf; Juhász, Béla; Balla, György; Szilvássy, Zoltán; Balla, József; Gáll, Tamás

doi:10.3390/ijms22179263

Cited by 4 publications

(2 citation statements)

References 62 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Terpinen-4-ol hinders posttranslational PERK formation at the K889 acetylation site by increasing SIRT1 expression and improving VC by regulating the ER pressure [ 89 ]. Interleukin enhancer binding factor 3 (ILF3) expression was found to be increased in calcified human aortic vascular smooth muscle cells (HAVSMCs) and calcified atherosclerotic plaques in humans and mice, and ILF3 promoted atherosclerotic calcification by acting on the promoter regions of BMP2 and STAT1 and mediating BMP2 upregulation and STAT1 downregulation, according to Fei Xie et al [ 90 ] BGP-15 is an emerging antidiabetic drug that has been found to inhibit Pi-induced phenotypic transformation during the osteochondrogenesis and mineralization of VSMCs, making it potentially ideal for reducing diabetic and nondiabetic vascular calcification [ 91 ]. In vitro experiments demonstrated that miR-223-3p blocked interleukin 6 (IL-6)/STAT3 signaling, thereby preventing osteogenic transformation and calcification in VSMCs [ 92 ].…”

Section: Cardiovascular Diseases Associated With Vsmcs Phenotypic Swi...mentioning

confidence: 99%

Vascular Smooth Muscle Cells Phenotypic Switching in Cardiovascular Diseases

Tang

Chen

Zhang

et al. 2022

Cells

View full text Add to dashboard Cite

Vascular smooth muscle cells (VSMCs), the major cell type in the arterial vessel wall, have a contractile phenotype that maintains the normal vessel structure and function under physiological conditions. In response to stress or vascular injury, contractile VSMCs can switch to a less differentiated state (synthetic phenotype) to acquire the proliferative, migratory, and synthetic capabilities for tissue reparation. Imbalances in VSMCs phenotypic switching can result in a variety of cardiovascular diseases, including atherosclerosis, in-stent restenosis, aortic aneurysms, and vascular calcification. It is very important to identify the molecular mechanisms regulating VSMCs phenotypic switching to prevent and treat cardiovascular diseases with high morbidity and mortality. However, the key molecular mechanisms and signaling pathways participating in VSMCs phenotypic switching have still not been fully elucidated despite long-term efforts by cardiovascular researchers. In this review, we provide an updated summary of the recent studies and systematic knowledge of VSMCs phenotypic switching in atherosclerosis, in-stent restenosis, aortic aneurysms, and vascular calcification, which may help guide future research and provide novel insights into the prevention and treatment of related diseases.

show abstract

Section: Cardiovascular Diseases Associated With Vsmcs Phenotypic Swi...mentioning

confidence: 99%

Vascular Smooth Muscle Cells Phenotypic Switching in Cardiovascular Diseases

Tang

Chen

Zhang

et al. 2022

Cells

View full text Add to dashboard Cite

show abstract

“…Chen et al [ 306 ] showed that the calcium channel blocker verapamil inhibited the production and activity of calcifying EVs and also reduced the calcifying capacity of COL 1 to prevent ECM mineralization. BGP-15 is a new anti-diabetic drug candidate that increased MGP content and decreased Annexin A2 content in EVs and prevented calcium deposition in the ECM [ 307 ]. Alendronate (ALE), a bone resorption inhibitor, down-regulated the release of aged bone-EVs in VD3-treated aged mice to reduce the ovariectomy-induced VC [ 10 ].…”

Section: Treatment Strategy Of Vascular Calcification Based On "Cross...mentioning

confidence: 99%

Vascular calcification: from the perspective of crosstalk

Yang,

Zeng,

Yuan

et al. 2023

Mol Biomed

View full text Add to dashboard Cite

Vascular calcification (VC) is highly correlated with cardiovascular disease morbidity and mortality, but anti-VC treatment remains an area to be tackled due to the ill-defined molecular mechanisms. Regardless of the type of VC, it does not depend on a single cell but involves multi-cells/organs to form a complex cellular communication network through the vascular microenvironment to participate in the occurrence and development of VC. Therefore, focusing only on the direct effect of pathological factors on vascular smooth muscle cells (VSMCs) tends to overlook the combined effect of other cells and VSMCs, including VSMCs-VSMCs, ECs-VMSCs, Macrophages-VSMCs, etc. Extracellular vesicles (EVs) are a collective term for tiny vesicles with a membrane structure that are actively secreted by cells, and almost all cells secrete EVs. EVs docked on the surface of receptor cells can directly mediate signal transduction or transfer their contents into the cell to elicit a functional response from the receptor cells. They have been proven to participate in the VC process and have also shown attractive therapeutic prospects. Based on the advantages of EVs and the ability to be detected in body fluids, they may become a novel therapeutic agent, drug delivery vehicle, diagnostic and prognostic biomarker, and potential therapeutic target in the future. This review focuses on the new insight into VC molecular mechanisms from the perspective of crosstalk, summarizes how multi-cells/organs interactions communicate via EVs to regulate VC and the emerging potential of EVs as therapeutic methods in VC. We also summarize preclinical experiments on crosstalk-based and the current state of clinical studies on VC-related measures.

show abstract