ArticleCommunications biology2024
MicroRNA-221-3p inhibits the inflammatory response of keratinocytes by regulating the DYRK1A/STAT3 signaling pathway to promote wound healing in diabetes.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 34 citations in OpenAlex.
- The Wound-Heart Axis: Can Chronic Wounds Contribute to Cardiac Dysfunction?International journal of molecular sciences · 2026Review
- Exosomes in precision dermatology: From biomarkers to targeted therapeutics in personalized care.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026Review
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- Targeting NAT10 alleviates colonic senescence and elderly-onset colitis by disrupting N4-acetylation of DYRK1A.Nature communications · 2026Article
- Bioengineered probiotics derived bacterial extracellular vesicle as bioactive nanocarrier for the local VEGF expression to accelerate wound healing.Journal of nanobiotechnology · 2026Article
- Article
- Review
- miR-191-5p inhibits angiogenesis in diabetic foot ulcers wound healing via regulating VEGFA.European journal of medical research · 2025Article
- Function of epigenetic modifications in wound healing and potential therapies (Review).International journal of molecular medicine · 2025Review
- MiR-221-3p Attenuates IL-33-Induced Mast Cell Cytokine Expression by Targeting KIT.International forum of allergy & rhinology · 2025Article
- Understanding molecular mechanism of diabetic wound healing: addressing recent advancements in therapeutic managements.Journal of diabetes and metabolic disorders · 2025Review
- The PVT1-214/miR-671-5p/SLC45A4 signaling axis regulates cell proliferation in human gastric cancer.World journal of surgical oncology · 2025Article
- Article
- DYRK1A in blood and immune function: implications in leukemia, inflammatory disorders, infection and Down syndrome.Frontiers in cell and developmental biology · 2025Review
- An analysis of gene expression profiles through machine learning uncovers the new diagnostic signature for diabetic foot ulcers.Frontiers in genetics · 2025Article
- New insights into microRNA in dermatological diseases.Frontiers in medicine · 2025Review
- A miRNA cocktail orchestrates coordinated cellular responses to promote diabetic wound healing.Burns & trauma · 2025Article
- Exosomal non-coding RNAs: a new avenue for treating diabetic foot ulcers.Frontiers in molecular biosciences · 2025Review
- Transcriptomics Revealed Differentially Expressed Transcription Factors and MicroRNAs in Human Diabetic Foot Ulcers.Proteomes · 2024Article
- Translational Challenges in Drug Therapy and Delivery Systems for Treating Chronic Lower Extremity Wounds.Pharmaceutics · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Diabetic foot ulcer (DFU), a serious complication of diabetes, remains a clinical challenge. MicroRNAs affect inflammation and may have therapeutic value in DFU. Here, we find that an miR-221-3p mimic reduces the inflammatory response and increases skin wound healing rates in a mouse model of diabetes, whereas miR-221-3p knockout produced the opposite result. In human keratinocytes cells, miR-221-3p suppresses the inflammatory response induced by high glucose. The gene encoding DYRK1A is a target of miR-221-3p. High glucose increases the expression of DYRK1A, but silencing DYRK1A expression decreases high glucose-induced inflammatory cytokine release via dephosphorylation of STAT3, a substrate of DYRK1A. Application of miR-221-3p mimic to human keratinocytes cells not only decreases DYRK1A expression but also inhibits high glucose-induced production of inflammatory cytokines to promote wound healing. This molecular mechanism whereby miR-221-3p regulates inflammation through the DYRK1A/STAT3 signaling pathway suggests targets and therapeutic approaches for treating DFU.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.