ArticleProceedings of the National Academy of Sciences of the United States of America2017
Interleukin-37 suppresses the osteogenic responses of human aortic valve interstitial cells in vitro and alleviates valve lesions in mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 114 citations in OpenAlex.
- Aortic valve disease: Novel animal models for advancing our understanding of the underlying mechanisms.Animal models and experimental medicine · 2026Review
- Association of Non-Insulin-Based Insulin Resistance Indices With Risk of Incident Valvular Heart Disease: Results From the UK Biobank Cohort Study.Journal of the American Heart Association · 2025Article
- Macrophages as key modulators of calcific aortic valve disease.Frontiers in cardiovascular medicine · 2025Review
- Th1 cells reduce the osteoblast-like phenotype in valvular interstitial cells by inhibiting NLRP3 inflammasome activation in macrophages.Molecular medicine (Cambridge, Mass.) · 2024Article
- Advanced glycation end product-modified low-density lipoprotein promotes pro-osteogenic reprogramming via RAGE/NF-κB pathway and exaggerates aortic valve calcification in hamsters.Molecular medicine (Cambridge, Mass.) · 2024Article
- Molecular Interaction of Soluble Klotho with FGF23 in the Pathobiology of Aortic Valve Lesions Induced by Chronic Kidney Disease.International journal of biological sciences · 2024Article
- Inflammation-associated ectopic mineralization.Fundamental research · 2023Review
- Targeted inhibition of PTPN22 is a novel approach to alleviate osteogenic responses in aortic valve interstitial cells and aortic valve lesions in mice.BMC medicine · 2023Article
- The Complex Relationship between Hypoxia Signaling, Mitochondrial Dysfunction and Inflammation in Calcific Aortic Valve Disease: Insights from the Molecular Mechanisms to Therapeutic Approaches.International journal of molecular sciences · 2023Review
- Toll-Like Receptor 3 Mediates Aortic Stenosis Through a Conserved Mechanism of Calcification.Circulation · 2023Article
- Interleukin-37 suppresses the cytotoxicity of hepatitis B virus peptides-induced CD8+ T cells in patients with acute hepatitis B.Biomolecules & biomedicine · 2023Article
- Recombinant IL-37 Exerts an Anti-inflammatory Effect on Human Aortic Valve Interstitial Cells through Extracellular and Intracellular Actions.International journal of biological sciences · 2023Article
- Mechanical injury accentuates lipid deposition in ApoEFrontiers in cardiovascular medicine · 2023Article
- [Optimal time window for observation of calcific aortic valve disease in mice following catheter-induced valve injury].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Interleukin 38 alleviates aortic valve calcification by inhibition of NLRP3.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Molecular Imaging of Aortic Valve Stenosis with Positron Emission Tomography.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Monocytes augment inflammatory responses in human aortic valve interstitial cells via βInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Role of oxidative stress in calcific aortic valve disease and its therapeutic implications.Cardiovascular research · 2022Review
- Pro-inflammatory mediators released by activated monocytes promote aortic valve fibrocalcific activity.Molecular medicine (Cambridge, Mass.) · 2022Article
- The intellectual base and research fronts of IL-37: A bibliometric review of the literature from WoSCC.Frontiers in immunology · 2022Review
5 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 3 institutions in 3 countries.
Funding
Abstract
Calcific aortic valve disease is a chronic inflammatory process, and aortic valve interstitial cells (AVICs) from diseased aortic valves express greater levels of osteogenic factors in response to proinflammatory stimulation. Here, we report that lower cellular levels of IL-37 in AVICs of diseased human aortic valves likely account for augmented expression of bone morphogenetic protein-2 (BMP-2) and alkaline phosphatase (ALP) following stimulation of Toll-like receptor (TLR) 2 or 4. Treatment of diseased AVICs with recombinant human IL-37 suppresses the levels of BMP-2 and ALP as well as calcium deposit formation. In mice, aortic valve thickening is observed when exposed to a TLR4 agonist or a high fat diet for a prolonged period; however, mice expressing human IL-37 exhibit significantly lower BMP-2 levels and less aortic valve thickening when subjected to the same regimens. A high fat diet in mice results in oxidized low-density lipoprotein (oxLDL) deposition in aortic valve leaflets. Moreover, the osteogenic responses in human AVICs induced by oxLDL are suppressed by recombinant IL-37. Mechanistically, reduced osteogenic responses to oxLDL in human AVICs are associated with the ability of IL-37 to inhibit NF-κB and ERK1/2. These findings suggest that augmented expression of osteogenic factors in AVICs of diseased aortic valves from humans is at least partly due to a relative IL-37 deficiency. Because recombinant IL-37 suppresses the osteogenic responses in human AVICs and alleviates aortic valve lesions in mice exposed to high fat diet or a proinflammatory stimulus, IL-37 has therapeutic potential for progressive calcific aortic valve disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.