ArticleMolecules and cells2022
The Molecular Mechanism of Long Non-Coding RNA MALAT1-Mediated Regulation of Chondrocyte Pyroptosis in Ankylosing Spondylitis.
Article in Molecules and cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- The role of exosomes in ankylosing spondylitis: from biological features and functional cargo to clinical applications.Frontiers in molecular biosciences · 2026Review
- The regulating markers for Brucella spondylitis and tuberculous spondylitis.BMC infectious diseases · 2025Article
- Aberrant bone formation and dysregulated bone homeostasis in ankylosing spondylitis.World journal of stem cells · 2025Article
- Potential Regulation of the Long Non-Coding RNA Metastasis-Associated Lung Adenocarcinoma Transcript1 by Estrogen in Parkinson's Disease.Life (Basel, Switzerland) · 2024Review
- Research progress on long non‑coding RNAs in non‑infectious spinal diseases (Review).Molecular medicine reports · 2024Review
- Identification and bioinformatics analysis of lncRNAs in serum of patients with ankylosing spondylitis.BMC musculoskeletal disorders · 2024Review
- Acrylamide induces human chondrocyte cell death by initiating autophagy‑dependent ferroptosis.Experimental and therapeutic medicine · 2023Article
- Knockdown of the long non‑coding RNA MALAT1 ameliorates TNF‑α‑mediated endothelial cell pyroptosis via the miR‑30c‑5p/Cx43 axis.Molecular medicine reports · 2023Article
- Novel regulatory role of non-coding RNAs in ankylosing spondylitis.Frontiers in immunology · 2023Review
- The regulatory activities of MALAT1 in the development of bone and cartilage diseases.Frontiers in endocrinology · 2022Review
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Authors and funding
5 authors.
Funding
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Abstract
Long non-coding RNAs (lncRNAs) may be important regulators in the progression of ankylosing spondylitis (AS). The competing endogenous RNA (ceRNA) activity of lncRNAs plays crucial roles in osteogenesis. We identified the mechanism of the differentially expressed lncRNA MALAT1 in AS using bioinformatic analysis and its ceRNA mechanism. The interaction of MALAT1, microRNA-558, and GSDMD was identified using integrated bioinformatics analysis and validated. Loss- and gain-of-function assays evaluated their effects on the viability, apoptosis, pyroptosis and inflammation of chondrocytes in AS. We found elevated MALAT1 and GSDMD but reduced miR-558 in AS cartilage tissues and chondrocytes. MALAT1 contributed to the suppression of cell viability and facilitated apoptosis and pyroptosis in AS chondrocytes. GSDMD was a potential target gene of miR-558. Depletion of MALAT1 expression elevated miR-558 by inhibiting GSDMD to enhance cell viability and inhibit inflammation, apoptosis and pyroptosis of chondrocytes in AS. In summary, our key findings demonstrated that knockdown of MALAT1 served as a potential suppressor of AS by upregulating miR-558 via the downregulation of GSDMD expression.
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