ArticleJournal of cellular and molecular medicine2022
TNFα activation and TGFβ blockage act synergistically for smooth muscle cell calcification in patients with venous thrombosis via TGFβ/ERK pathway.
Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Transforming Growth Factors in Venous Thrombus Formation and Resolution.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- A Rare Case of Linear Phlebolith: Foreign Body Discovered in the Femoral Vein.Case reports in surgery · 2025Article
- miR-2467-3p/ABLIM1 Axis Mediates the Formation and Progression of Deep Vein Thrombosis by Regulating Inflammation and Oxidative Stress.The International journal of angiology : official publication of the International College of Angiology, Inc · 2024Article
- Potential actions of capsaicin for preventing vascular calcification of vascular smooth muscle cellsHeliyon · 2024Article
- Vascular Calcification: Molecular Networking, Pathological Implications and Translational Opportunities.Biomolecules · 2024Review
- Diagnostic and prognostic potential of long non-coding RNA NORAD in patients with acute deep vein thrombosis and its role in endothelial cell function.Thrombosis journal · 2024Article
- Exploring molecular profiles of calcification in aortic vascular smooth muscle cells and aortic valvular interstitial cells.Journal of molecular and cellular cardiology · 2023Article
- TNFα activation and TGFβ blockage act synergistically for smooth muscle cell calcification in patients with venous thrombosis via TGFβ/ERK pathway.Journal of cellular and molecular medicine · 2022Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Venous calcification has been observed in post-thrombotic syndrome (PTS) patients; yet, the cell types and possible mechanisms regulating this process are still unclear. We evaluated the calcium deposition within the venous wall, the cell type involved in the calcified remodelling of the venous wall after thrombosis and explored possible mechanisms in vitro. Calcium deposition was found in human specimens of superficial thrombotic veins and was co-localized with VSMCs markers αSMA and TAGLN (also known as SM22α). Besides, the expression of osteogenesis-related genes was dramatically changed in superficial thrombotic veins. Moreover, the inhibition of the TGFβ signalling pathway after TNFα treatment effectively induced the expression of osteogenic phenotype markers, the calcium salt deposits and the obvious phosphorylation of ERK1/2 and JNK2 in the VSMCs calcification model. Supplementing TGFβ2 or blocking the activation of the ERK/MAPK signalling pathway prevented the transformation of VSMCs into osteoblast-like cells in vitro. Taken together, VSMCs have an important role in venous calcification after thrombosis. Supplementing TGFβ2 or inhibiting the ERK/MAPK signalling pathway can reduce the appearance of VSMCs osteogenic phenotype. Our findings may present a novel therapeutic approach to prevent of vascular calcification after venous thrombosis.
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