ReviewCell proliferation2022
Novel insights into the interaction between N6-methyladenosine methylation and noncoding RNAs in musculoskeletal disorders.
Review in Cell proliferation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 50 citations in OpenAlex.
- The progress of m6A methylation-regulated non-coding RNAs in osteogenic differentiation and osteoporosis.Non-coding RNA research · 2026Review
- METTL3-mediated GLUD1 m6A Modification Promotes Hydrogen Peroxide-induced Mitochondrial Dysfunction in Human Nucleus Pulposus Cells Via the Glutamate/α-KG Metabolic Axis.Journal of musculoskeletal & neuronal interactions · 2026Article
- METTL3-mediated mAnnals of medicine · 2025Article
- METTL3 inhibits osteoporosis by promoting osteoblast differentiation through m6A-mediated activation of the FZD3/RUNX1 signaling axis.European journal of medical research · 2025Article
- Peptide Drug: Design and Clinical Applications.MedComm · 2025Review
- FTO-mediated MMP1 m6A modification promotes osteogenic differentiation of bone marrow mesenchymal stem cells via the ERK pathway in congenital scoliosis.Scientific reports · 2025Article
- NJournal of orthopaedic translation · 2025Review
- Deciphering the etiology of congenital scoliosis: A genetic and epigenetic perspective.World journal of orthopedics · 2025Review
- Crosstalk between N6-methyladenosine modification and ncRNAs in rheumatic diseases: therapeutic and diagnostic implications.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- From bone marrow mesenchymal stem cells to diseases: the crucial role of mStem cell research & therapy · 2025Review
- Novel lncRNA LncMSTRG.11341.25 Promotes Osteogenic Differentiation of Human Bone Marrow Stem Cells via the miR-939-5p/PAX8 Axis.Research (Washington, D.C.) · 2025Article
- Unraveling the Role of N6-Methylation Modification: From Bone Biology to Osteoporosis.International journal of medical sciences · 2025Review
- Novel Insights into the Regulatory Role of N6-Methyladenosine in the Pathogenesis and Clinical Treatment of Osteoarthritis: Research Status and Prospect.Journal of inflammation research · 2025Review
- Therapeutic prospects and potential mechanisms of Prdx6: as a novel target in musculoskeletal disorders.Frontiers in physiology · 2025Review
- N6-methyladenosine-modified circCDK14 promotes ossification of the ligamentum flavum via epigenetic modulation by targeting AFF4.Cellular and molecular life sciences : CMLS · 2024Article
- Epigenetic control of skeletal muscle atrophy.Cellular & molecular biology letters · 2024Review
- YTHDF2-Mediated m6A methylation inhibition by miR27a as a protective mechanism against hormonal osteonecrosis in BMSCs.BMC musculoskeletal disorders · 2024Article
- Novel Insights into the Links between N6-Methyladenosine and Regulated Cell Death in Musculoskeletal Diseases.Biomolecules · 2024Review
- Experimental validation and comprehensive analysis of m6A methylation regulators in intervertebral disc degeneration subpopulation classification.Scientific reports · 2024Article
- N6-methyladenosine reader protein IGF2BP1 suppresses CD8 + T cells-mediated tumor cytotoxicity and apoptosis in colon cancer.Apoptosis : an international journal on programmed cell death · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMusculoskeletal disorder (MSD) are a class of inflammatory and degener-ative diseases, but the precise molecular mechanisms are still poorly understood. Noncoding RNA (ncRNA) N6-methyladenosine (m6A) modification plays an essential role in the pathophysiological process of MSD. This review summarized the interaction between m6A RNA methylation and ncRNAs in the molecular regulatory mechanism of MSD. It provides a new perspective for the pathophysiological mechanism and ncRNA m6A targeted therapy of MSD.
methodsA comprehensive search of databases was conducted with musculoskeletal disorders, noncoding RNA, N6-methyladenosine, intervertebral disc degeneration, osteoporosis, osteosarcoma, osteoarthritis, skeletal muscle, bone, and cartilage as the key-words. Then, summarized all the relevant articles.
resultsIntervertebral disc degeneration (IDD), osteoporosis (OP), osteosarcoma (OS), and osteoarthritis (OA) are common MSDs that affect muscle, bone, cartilage, and joint, leading to limited movement, pain, and disability. However, the precise pathogenesis remains unclear, and no effective treatment and drug is available at present. Numerous studies confirmed that the mutual regulation between m6A and ncRNAs (i.e., microRNAs, long ncRNAs, and circular RNAs) was found in MSD, m6A modification can regulate ncRNAs, and ncRNAs can also target m6A regulators. ncRNA m6A modification plays an essential role in the pathophysiological process of MSDs by regulating the homeostasis of skeletal muscle, bone, and cartilage.
conclusionm6A interacts with ncRNAs to regulate multiple biological processes and plays important roles in IDD, OP, OS, and OA. These studies provide new insights into the pathophysiological mechanism of MSD and targeting m6A-modified ncRNAs may be a promising therapy approach.
Indexed as
Identifiers
What Socratic 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 Socratic graph.