ArticleAmerican journal of translational research2021
A decrease in IL-33 regulates matrix degradation and apoptosis in intervertebral disc degeneration via HIF-1alpha.
Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- A Bibliometric Study of Interleukin Cytokines in the Treatment of Intervertebral Disc Degeneration.Drug design, development and therapy · 2025Article
- Blood-nerve barrier enhances chronic postsurgical pain via the HIF-1α/ aquaporin-1 signaling axis.BMC anesthesiology · 2023Article
- Intervertebral disc degeneration and inflammatory microenvironment: expression, pathology, and therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Pulsed Electromagnetic Field Alleviates Intervertebral Disc Degeneration by Activating Sirt1-Autophagy Signaling Network.Frontiers in bioengineering and biotechnology · 2022Article
- Decreased intracellular IL-33 impairs endometrial receptivity in women with adenomyosis.Frontiers in endocrinology · 2022Article
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
Low back pain (LBP) is a common aging-associated disease that can cause disability in old people. Previous research revealed that an imbalance in the extracellular matrix (ECM) via abnormal hypoxia-inducible factor-1alpha (HIF-1α) expression in nucleus pulposus (NP) cells was one of the key factors in the pathogenesis of intervertebral disc degeneration (IDD). However, the mechanism by which the ECM is reduced in patients with IDD is not fully understood. Here, we reported that a new member of the interleukin (IL)-1 family, IL-33, was positively correlated with HIF-1α and was decreased in the NP cells of individuals with IDD. IL-33 overexpression in degenerative NP cells decreased the levels of matrix metalloproteinase-3/13 (MMP-3/13), a disintegrin and metallo-proteinase with thrombospondin motifs-4/5 (ADAMTS-4/5), and promoted ECM expression in vitro. Furthermore, we preliminarily explored the antiapoptotic effects of IL-33, which could reduce the expression of Caspase-3 and promote the level of Bcl-2 in degenerative NP cells. Furthermore, when HIF-1α expression was silenced, IL-33-mediated upregulation of ECM expression was weakened. Thus, IL-33-induced HIF-1α upregulation may represent a novel therapeutic strategy to ameliorate IDD in patients with LBP.
Indexed as
Identifiers
34956487PMC8661207W4206895075What OpenQuestion holds
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.