ArticleMolecular medicine reports2017
High mobility group box 1 induces calcification of aortic valve interstitial cells via toll-like receptor 4.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Tissue and Serum Biomarkers in Degenerative Aortic Stenosis-Insights into Pathogenesis, Prevention and Therapy.Biology · 2023Article
- High-mobility group box-1 promotes vascular calcification in diabetic mice via endoplasmic reticulum stress.Journal of cellular and molecular medicine · 2021Article
- Recombinant high‑mobility group box 1 induces cardiomyocyte hypertrophy by regulating the 14‑3‑3η, PI3K and nuclear factor of activated T cells signaling pathways.Molecular medicine reports · 2021Article
- Deregulation of TLR4 signaling pathway characterizes Bicuspid Aortic valve syndrome.Scientific reports · 2019Article
- Associations of severity of fatty liver with oxidative stress, SAA, CRP and degree of cerebral arteriosclerosis in cerebral arteriosclerosis patients who have fatty liver.International journal of clinical and experimental pathology · 2019Article
- Toll-Like Receptors, Inflammation, and Calcific Aortic Valve Disease.Frontiers in physiology · 2018Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic inflammation and the calcification of aortic valve interstitial cells (AVICs) are the primary etiologies of calcific aortic valve disease (CAVD). However, the underlying mechanism remains to be elucidated. The present study investigated the importance of high mobility group box 1 (HMGB1) via toll‑like receptor 4 (TLR4) for the regulation of inflammation and calcification in AVICs. It was determined that the expression levels of HMGB1 and TLR4 were increased in the calcific region of aortic valves with CAVD. In cultured primary AVICs from wild‑type mice, HMGB1 treatment demonstrated a dose-dependent increase in mineralization levels and osteogenic gene expression. These effects were significantly reduced in AVICs obtained from TLR4 knockout mice (TLR4‑/‑). In addition, calcification was inhibited by TLR4-specific antibodies in primary AVICs. HMGB1 induced the activation of p38 and nuclear factor-κB (NF-κB) in TLR4‑/‑ primary AVICs, and inhibited p38 and NF‑κB in wild‑type AVICs treated with TLR4‑specific antibodies. The present study demonstrated that TLR4 may function as an essential mediator of HMGB1‑induced calcification and in the activation of p38 and NF-κB.
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Registered trials
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.