ArticleBiomedicines2021
Heme-Mediated Activation of the Nrf2/HO-1 Axis Attenuates Calcification of Valve Interstitial Cells.
Article in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Article
- Nogo-B attenuates vascular calcification by activating NRF2-SLC7A11 to enhance antioxidant defense.Redox biology · 2026Article
- Targeted proteomics reveals immune protein patterns in serum from patients with calcific aortic stenosis.iScience · 2025Article
- Iron in Vascular Calcification: Pro-Calcific Agent or Protective Modulator?International journal of molecular sciences · 2025Review
- Valvular calcification in chronic kidney disease: new insights from recent clinical and preclinical studies.Clinical kidney journal · 2025Article
- Association of Serum Total Bilirubin Level With Abdominal Aortic Calcification: A Population-Based Cross-Sectional Study.Mediators of inflammation · 2025Article
- β-Hydroxybutyrate Alleviates Atherosclerotic Calcification by Inhibiting Endoplasmic Reticulum Stress-Mediated Apoptosis via AMPK/Nrf2 Pathway.Nutrients · 2024Article
- MCL restrained ROS/AKT/ASAH1 pathway to therapy tamoxifen resistance breast cancer by stabilizing NRF2.Cell proliferation · 2024Article
- In Vitro Models of Cardiovascular Calcification.Biomedicines · 2024Review
- Morusin Alleviates Aortic Valve Calcification by Inhibiting Valve Interstitial Cell Senescence Through Ccnd1/Trim25/Nrf2 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Effect of iron administration on the aortic iron content and vascular calcification in phosphorus-loaded chronic kidney disease rats.BMC nephrology · 2023Article
- Empagliflozin Attenuates Vascular Calcification in Mice with Chronic Kidney Disease by Regulating the NFR2/HO-1 Anti-Inflammatory Pathway through AMPK Activation.International journal of molecular sciences · 2023Article
- Pathophysiology and Clinical Impacts of Chronic Kidney Disease on Coronary Artery Calcification.Journal of cardiovascular development and disease · 2023Review
- Review
- The dual role and mutual dependence of heme/HO-1/Bach1 axis in the carcinogenic and anti-carcinogenic intersection.Journal of cancer research and clinical oncology · 2023Review
- Hesperetin, a Promising Dietary Supplement for Preventing the Development of Calcific Aortic Valve Disease.Antioxidants (Basel, Switzerland) · 2022Article
- Review
- Activation of Nrf2/HO-1 Antioxidant Pathway by Heme Attenuates Calcification of Human Lens Epithelial Cells.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Heme in Cardiovascular Diseases: A Ubiquitous Dangerous Molecule Worthy of Vigilance.Frontiers in cell and developmental biology · 2021Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Calcific aortic valve stenosis (CAVS) is a heart disease characterized by the progressive fibro-calcific remodeling of the aortic valves, an actively regulated process with the involvement of the reactive oxygen species-mediated differentiation of valvular interstitial cells (VICs) into osteoblast-like cells. Nuclear factor erythroid 2-related factor 2 (Nrf2) regulates the expression of a variety of antioxidant genes, and plays a protective role in valve calcification. Heme oxygenase-1 (HO-1), an Nrf2-target gene, is upregulated in human calcified aortic valves. Therefore, we investigated the effect of Nrf2/HO-1 axis in VIC calcification. We induced osteogenic differentiation of human VICs with elevated phosphate and calcium-containing osteogenic medium (OM) in the presence of heme. Heme inhibited Ca deposition and OM-induced increase in alkaline phosphatase and osteocalcin (OCN) expression. Heme induced Nrf2 and HO-1 expression in VICs. Heme lost its anti-calcification potential when we blocked transcriptional activity Nrf2 or enzyme activity of HO-1. The heme catabolism products bilirubin, carbon monoxide, and iron, and also ferritin inhibited OM-induced Ca deposition and OCN expression in VICs. This study suggests that heme-mediated activation of the Nrf2/HO-1 pathway inhibits the calcification of VICs. The anti-calcification effect of heme is attributed to the end products of HO-1-catalyzed heme degradation and ferritin.
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