Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

ALKBH5‐mediated m6A demethylation ameliorates extracellular matrix deposition in cutaneous pathological fibrosis

1 Sept 2024

Abstract excerpt

Abstract Background Elevated extracellular matrix (ECM) accumulation is a major contributing factor to the pathogenesis of fibrotic diseases. Recent studies have indicated that N6‐methyladenosine (m6A) RNA modification plays a pivotal role in modulating RNA stability and contribute to the initiation of various pathological conditions. Howbeit, the precise mechanism by which m6A influences ECM deposition remains...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Autophagy in Disease and Therapy
Share to Peptidase Inhibition and Analysis
Share to RNA modifications and cancer

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 39233335
DOI: 10.1002/ctm2.70016

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

ALKBH5‐mediated m6A demethylation ameliorates extracellular matrix deposition in cutaneous pathological fibrosisPMID 39233335Read ↗

Epigenetic orchestration of RNA m6A methylation in wound healing and post-wound eventsSemantic proximity Read ↗

N6-methyladenosine (m6A) RNA modification in fibrosis and collagen-related diseasesSemantic proximity Read ↗

ALKBH5 Regulates Corneal Neovascularization by Mediating FOXM1 M6A DemethylationSemantic proximity Read ↗

Overexpression of LncRNA AC067945.2 Down-Regulates Collagen Expression in Skin Fibroblasts and Possibly Correlates with the VEGF and Wnt Signalling PathwaysSemantic proximity Read ↗

Genomics of Human Fibrotic Diseases: Disordered Wound Healing ResponseSemantic proximity Read ↗

Fibrosis—the tale of H3K27 histone methyltransferases and demethylasesSemantic proximity Read ↗

HDAC5-mediated Smad7 silencing through MEF2A is critical for fibroblast activation and hypertrophic scar formationSemantic proximity Read ↗

Epigenetic modification mechanisms involved in keloid: current status and prospectSemantic proximity Read ↗

Suppression of m6A mRNA modification by DNA hypermethylated ALKBH5 aggravates the oncological behavior of KRAS mutation/LKB1 loss lung cancer.Semantic proximity Read ↗

BMP1 Promotes Keloid by Inducing Fibroblast Inflammation and FibrogenesisSemantic proximity Read ↗

Inhibition of CUB and sushi multiple domains 1 (CSMD1) expression by miRNA-190a-3p enhances hypertrophic scar-derived fibroblast migration in vitroSemantic proximity Read ↗

LKB1 Loss Upregulates ALKBH5 and Contributes to Aggressive Phenotypes of KRAS Mutated Lung CancerSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.