ArticleAging2022
Galectin-3 induces vascular smooth muscle cells calcification via AMPK/TXNIP pathway.
Article in Aging, 2022. 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.
- Pleiotropic regulatory mechanisms and targeted therapeutic prospects of Galectin-3 in aging-related diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Smooth muscle cell-specific deletion of TXNIP ameliorates medial vascular calcification.Experimental & molecular medicine · 2025Article
- Virgin and photo-degraded microplastics induce the activation of human vascular smooth muscle cells.Scientific reports · 2025Article
- A novel application perspective of the clinical-used drug verapamil on osteoporosis via targetingJournal of orthopaedic translation · 2025Article
- Understanding Galectin-3's Role in Diastolic Dysfunction: A Contemporary Perspective.Life (Basel, Switzerland) · 2024Review
- Relationships between systemic sclerosis and atherosclerosis: screening for mitochondria-related biomarkers.Frontiers in genetics · 2024Article
- Role of galectin-3 in vascular calcification.Glycoconjugate journal · 2023Review
- TXNIP Suppresses the Osteochondrogenic Switch of Vascular Smooth Muscle Cells in Atherosclerosis.Circulation research · 2023Article
- The Endothelial Transcription Factor ERG Mediates a Differential Role in the Aneurysmatic Ascending Aorta with Bicuspid or Tricuspid Aorta Valve: A Preliminary Study.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Galectin-3 plays an important role in atherosclerosis. Upregulation of VSMCs calcification is involved in the progression and development of vulnerable plaques. Thioredoxin-interacting protein (TXNIP) has been regarded as an important determinant in regulating inflammation and oxidative stress. In this study, we evaluated the role of TXNIP in galectin-3-induced vascular calcification. A primary culture of mouse VSMCs was established by enzymatic digestion of aorta. Small interfering (si) RNA was used to knock down the expression of target gene. VSMCs were treated with 3-methyladenine (3-MA) or compound C respectively. Western blot was performed to detect the protein level in VSMCs, Alkaline phosphatase (ALP) and Alizarin red staining was used to observe calcium deposition. Dihydroethidium (DHE) staining was used to observe the reactive oxygen species (ROS) production. Here we showed that galectin-3 increased aorta and VSMCs calcification, which was associated with AMPK/TXNIP upregulation and autophagy activation. TXNIP inhibition decreased galectin-3-induced aorta and VSMCs calcification and autophagy activation. 3-MA or Atg5 siRNA decreased galectin-3-induced upregulation of Runx2, BMP2 and OPN. AMPK mediated galectin-3-induced VSMCs osteogenic differentiation. These findings illustrated that TXNIP mediated galectin-3-induced vascular calcification, AMPK and autophagy activation were also associated with this process.
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