ArticleClinical hypertension2015
Mesoglycan attenuates VSMC proliferation through activation of AMP-activated protein kinase and mTOR.
Article in Clinical hypertension, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Mesoglycan for long-term secondary prevention in patients with superficial vein thrombosis (METRO): a multicentre randomised clinical trial in Italy.EClinicalMedicine · 2026Article
- Procyanidin B2-induced LKB1-AMPK activation mitigates vascular smooth muscle cell proliferation through inhibition of mTOR signaling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- Article
- Clinical evidence and rationale of mesoglycan to treat chronic venous disease and hemorrhoidal disease: a narrative review.Updates in surgery · 2024Review
- Restoring the Platelet miR-223 by Calpain Inhibition Alleviates the Neointimal Hyperplasia in Diabetes.Frontiers in physiology · 2020Article
- ENPP1-Fc prevents neointima formation in generalized arterial calcification of infancy through the generation of AMP.Experimental & molecular medicine · 2018Article
- Combination treatment of adipose-derived stem cells and adiponectin attenuates pulmonary arterial hypertension in rats by inhibiting pulmonary arterial smooth muscle cell proliferation and regulating the AMPK/BMP/Smad pathway.International journal of molecular medicine · 2018Article
- The inhibitory effect of Isoliquiritigenin on the proliferation of human arterial smooth muscle cell.BMC pharmacology & toxicology · 2017Article
- Folic acid inhibits dedifferentiation of PDGF-BB-induced vascular smooth muscle cells by suppressing mTOR/P70S6K signaling.American journal of translational research · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundVascular smooth muscle cells (VSMC) proliferation contributes significantly to intimal thickening in atherosclerosis and restenosis diseases. Platelet derived growth factor (PDGF) has been implicated in VSMC proliferation though the activation of multiple growth-promoting signals. Mesoglycan, a natural glycosaminoglycans preparation, is reported to show vascular protective effect. However, the mechanisms by which mesoglycan inhibits proliferation of VSMC are not fully understood. Here, we investigated whether mesoglycan exert therapeutic effect via AMP-activated protein kinase (AMPK) and its underlying mechanism.
methodsWe cultured VSMC with increasing doses of mesoglycan. AMPK activation was measured by western blot analysis and cell proliferation was measured by flow cytometry.
resultsMesoglycan dose- and time- dependently increased the phosphorylation of AMPK (Thr(172)) and its upstream target, LKB1 (Ser(428)) and its downstream, ACC (Ser(79)) in VSMCs. Mesoglycan also blocked the PDGF-stimulated cell cycle progression through the G0/G1 arrest. AMPK DNα1, AMPK DNα2 or AMPK siRNA reduced the mesoglycan-mediated inhibition of VSMC proliferation. AMPK signaling activated by mesoglycan regulates mTOR phosphorylation which closely related to cell proliferation.
conclusionThese data suggest that mesoglycan-induced AMPK activation suppress the VSMC proliferation via mTOR-dependent mechanism and mesoglycan may have beneficial effects on vascular proliferative disorders such as atherosclerosis.
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