ArticleNature communications2019
RNA-binding protein ZFP36L1 regulates osteoarthritis by modulating members of the heat shock protein 70 family.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 88 citations in OpenAlex.
- Integrative analysis of cadmium exposure and osteoarthritis: from population evidence to molecular mechanisms.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Chiral FeBioactive materials · 2026Article
- ZFP36 inhibits the pro-apoptotic effects of transforming growth factor β1 on mitral valve interstitial cells via the GTP-binding protein 6 pathway in mitral valve prolapse.Experimental physiology · 2026Article
- Nanozyme-Integrated Hydrogel Targeting AGEs for Diabetic Osteoarthritis Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Impact of disease-associated chromatin accessibility QTLs across immune cell types and contexts.Cell genomics · 2026Article
- Potential molecular communication of blood and synovium through ligand-receptor interactions in osteoarthritis.Frontiers in medicine · 2026Article
- HSPA1A Can Alleviate CFA-Induced Inflammatory Pain by Modulating Macrophages.International journal of molecular sciences · 2025Article
- SIRT6 inhibits endoplasmic reticulum stress-mediated ferroptosis by activating Nrf2/HO-1 signaling to alleviate osteoarthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Heat shock proteins in osteoarthritis: molecular mechanisms, pathogenic roles, and therapeutic opportunities.Frontiers in immunology · 2025Review
- RNA-binding proteins regulate osteoarthritis via RNA metabolism regulation.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Review
- RNA-binding protein HNRNPD promotes chondrocyte senescence and osteoarthritis progression through upregulating FOXM1.Communications biology · 2024Article
- Recent Progress in the Research on RNA-Binding Proteins in Bone Development and Diseases.International journal of molecular sciences · 2024Review
- Enhancing Cartilage Metabolism in Rats through a Novel Thermal Stimulation Technique with Photosensitizers.International journal of molecular sciences · 2024Article
- A multifunctional nanogel encapsulating layered double hydroxide for enhanced osteoarthritis treatment via protection of chondrocytes and ECM.Materials today. Bio · 2024Article
- Identification and validation of biomarkers related to lipid metabolism in osteoarthritis based on machine learning algorithms.Lipids in health and disease · 2024Article
- Inhibitory effects of Acanthopanax sessiliflorus Harms extract on the etiology of rheumatoid arthritis in a collagen-induced arthritis mouse model.Arthritis research & therapy · 2024Article
- Network Analysis of Osteoarthritis Progression Using a Steiner Minimal Tree Algorithm.Journal of inflammation research · 2024Article
- NaNature · 2024Article
- Prokineticin 2 is a catabolic regulator of osteoarthritic cartilage destruction in mouse.Arthritis research & therapy · 2023Article
- Emerging roles of RNA binding proteins in intervertebral disc degeneration and osteoarthritis.Orthopaedic surgery · 2023Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is a whole-joint disease characterized by cartilage destruction and other whole-joint pathological changes. There is currently no effective disease-modifying therapy. Here we investigate the post-transcriptional mRNA regulation of OA-modulating proteins in chondrocytes and show that the ZFP36 family member, ZFP36L1, is specifically upregulated in OA chondrocytes and OA cartilage of humans and mice. Adenovirus-mediated overexpression of ZFP36L1 alone in mouse knee-joint tissue does not modulate OA pathogenesis. However, genetic ablation or silencing of Zfp36l1 significantly abrogates experimental OA in mice. Knockdown of Zfp36l1 increases the mRNA expression of two heat shock protein 70 (HSP70) family members, which act as its direct targets. Furthermore, overexpression of HSPA1A in joint tissues protects mice against experimental OA by inhibiting chondrocyte apoptosis. Our results indicate that the RNA-binding protein, ZFP36L1, regulates HSP70 family members that appear to protect against OA pathogenesis by inhibiting chondrocyte apoptosis.
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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.