ArticleClinical and translational medicine2024
ALKBH5-mediated m
Article in Clinical and translational medicine, 2024. 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.
- mExperimental and therapeutic medicine · 2026Review
- Epigenetic orchestration of scar formation: Therapeutic potential of targeting DNA methylation and non‑coding RNAs in cutaneous fibrosis (Review).Molecular medicine reports · 2026Review
- YTHDF1-Mediated m6A Modification of NREP Promotes Corneal Fibrosis via TGF-β-Smad Signaling.Investigative ophthalmology & visual science · 2026Article
- Identification of common genetic features and pathways for osteoporosis with frozen shoulder by integrated bioinformatics analysis and machine learning.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Article
- A compact five-gene immuno-fibrotic profile distinguishing systemic sclerosis subtypes with PXDN validated as a fibrosis-associated target.Frontiers in immunology · 2026Article
- Retinal ALKBH5 inhibition induces myopia protection through selective regulation of ERK1/2 signaling.Journal of translational medicine · 2025Article
- LINC01711 modulates proliferation, migration, and extracellular matrix deposition of hypertrophic scar fibroblasts by targeting miR-34a-5p.Archives of dermatological research · 2025Article
- Epigenetic orchestration of RNA mInternational journal of biological sciences · 2025Review
- Cell-free adipose extract inhibits hypertrophic scar formation through collagen remodeling and antiangiogenesis.Open medicine (Warsaw, Poland) · 2025Article
- ALKBH5-mediated mClinical and translational medicine · 2024Article
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Authors and funding
10 authors.
Funding
Abstract
backgroundElevated extracellular matrix (ECM) accumulation is a major contributing factor to the pathogenesis of fibrotic diseases. Recent studies have indicated that N6-methyladenosine (m
methodsIn this study, we used hypertrophic scars (HTSs) as a paradigm to investigate ECM-related diseases. We focused on the role of ALKBH5-mediated m
resultsALKBH5 was decreased in fibroblasts derived from HTS lesions and was negatively correlated with their clinical stages. Importantly, ablation of ALKBH5 promoted the expression of COL3A1, COL1A1, and ELN, leading to pathological deposition and reconstruction of the ECM both in vivo and in vitro. From a therapeutic perspective, the exogenous overexpression of ALKBH5 significantly inhibited abnormal collagen deposition in fibrotic scar models. As determined by integrated high-throughput analysis, key ECM components including COL3A1, COL1A1, and ELN are direct downstream targets of ALKBH5. By means of its mechanism, ALKBH5 inhibits the expression of COL3A1, COL1A1, and ELN by removing m
conclusionsOur study identified ALKBH5 as an endogenous suppressor of pathological ECM deposition, contributing to the development of a reprogrammed m6A-targeted therapy for HTSs.
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