ArticleAnnals of translational medicine2020
LncRNA FAM83H-AS1 maintains intervertebral disc tissue homeostasis and attenuates inflammation-related pain via promoting nucleus pulposus cell growth through miR-22-3p inhibition.
Article in Annals of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Multiomics Data Synthesis of FAM83H in Amelogenesis Imperfecta.International dental journal · 2026Pooled it
- Epigenetic research methods and animal models for intervertebral disc degeneration (Review).Molecular medicine reports · 2026Review
- Advanced Glycation End Products Induce Caudal Disc Degeneration in Ovariectomized Female Rats.JOR spine · 2025Article
- Research progress on long non‑coding RNAs in non‑infectious spinal diseases (Review).Molecular medicine reports · 2024Review
- Article
- Role of lncRNA MAGI2-AS3 in lipopolysaccharide-induced nucleus pulposus cells injury by regulating miR-374b-5p/interleukin-10 axis.Immunity, inflammation and disease · 2023Article
- Targeting Autophagy for Developing New Therapeutic Strategy in Intervertebral Disc Degeneration.Antioxidants (Basel, Switzerland) · 2022Review
- Mechanism of Long Noncoding RNA HOTAIR in Nucleus Pulposus Cell Autophagy and Apoptosis in Intervertebral Disc Degeneration.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Role of Advanced Glycation End Products in Intervertebral Disc Degeneration: Mechanism and Therapeutic Potential.Oxidative medicine and cellular longevity · 2022Review
- The potential mechanisms and application prospects of non-coding RNAs in intervertebral disc degeneration.Frontiers in endocrinology · 2022Review
- An Oxidative Stress-Related Gene Pair (Frontiers in immunology · 2021Article
- Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIntervertebral disc degeneration (IVDD) is regarded as the leading cause of low back pain, resulting in disability and a heavy burden on public health. Several studies have unveiled that long noncoding RNAs (lncRNAs) play a key role in the pathogenesis and progression of IVDD. In this study, we aimed to investigate the biological function and latent molecular mechanism of the lncRNA FAM83H antisense RNA 1 (FAM83H-AS1) in IVDD development.
methodsFirstly, we established an IVDD model in rats using advanced glycation end products (AGEs) intradiscal injection. Subsequently, gain-of-function assays were conducted to investigate the role of FAM83H-AS1 in the progression of IVDD. Bioinformatics analysis, RNA pull down assay and rescue experiments were employed to shed light on the molecular mechanism underlying FAM83H-AS1 involving in IVDD.
resultsOur findings verified that AGEs treatment aggravated IVDD damage, and FAM83H-AS1 was downregulated in the IVDD group. Additionally, overexpression of FAM83H-AS1 contributed to the growth of nucleus pulposus (NP) cells and ameliorated IVDD injury. It was revealed that FAM83H-AS1 possessed the speculated binding sites of miR-22-3p. More importantly, we confirmed that FAM83H-AS1 functioned as a sponge of miR-22-3p in IVDD. Lastly, we demonstrated that miR-22-3p mediated the impact of FAM83H-AS1 on cell proliferation, ECM degradation, and inflammation.
conclusionsOur study indicated that FAM83H-AS1 relieved IVDD deterioration through sponging miR-22-3p, and provides novel insights into the mechanisms underlying FAM83H-AS1 in IVDD progression.
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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.