ArticleThe Journal of investigative dermatology2015
miR-23a-3p causes cellular senescence by targeting hyaluronan synthase 2: possible implication for skin aging.
Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 73 citations in OpenAlex.
- Epigenetic regulation of hyaluronan degradation and melanogenesis by Kawarayomogin I and II from Artemisia capillaris via miR-486-5p and miR-141-3p.Molecular biology reports · 2026Article
- Circulating microRNAs miR-21-5p, miR-23a-3p and miR-26a-5p reflect clinical and molecular features of aging.Scientific reports · 2025Article
- Hyaluronic Acid in Topical Applications: The Various Forms and Biological Effects of a Hero Molecule in the Cosmetics Industry.Biomolecules · 2025Review
- Hyperoside Promotes Mitochondrial Autophagy Through the miR-361-5p/PI3K/Akt/mTOR Signaling Pathway, Thereby Improving UVB-Induced Photoaging.Antioxidants (Basel, Switzerland) · 2025Article
- The emerging role of miRNAs in biological aging and age-related diseases.Non-coding RNA research · 2025Review
- miR-23a-mediated TRF2 repression in CD4 T cells from PLWH.Molecular immunology · 2025Article
- Hyaluronic Acid and Skin: Its Role in Aging and Wound-Healing Processes.Gels (Basel, Switzerland) · 2025Review
- Epigenetics in Skin Homeostasis and Ageing.Epigenomes · 2025Review
- Elucidation of how the Mir-23-27-24 cluster regulates development and aging.Experimental & molecular medicine · 2024Review
- Extracellular vesicles derived from mesenchymal stem cells: the wine in Hebe's hands to treat skin aging.Precision clinical medicine · 2024Review
- Icariin Attenuates Human Renal Tubular Epithelial Cell Senescence by Targeting PAK2Current pharmaceutical biotechnology · 2024Article
- Review
- Article
- Identification and comprehensive analysis of circRNA-miRNA-mRNA regulatory networks in osteoarthritis.Frontiers in immunology · 2022Article
- Protective effects of galangin against HAging · 2021Article
- Targeting microRNA for improved skin health.Health science reports · 2021Review
- Antitumor effect of 4MU on glioblastoma cells is mediated by senescence induction and CD44, RHAMM and p-ERK modulation.Cell death discovery · 2021Article
- Review
- miR-23a/b suppress cGAS-mediated innate and autoimmunity.Cellular & molecular immunology · 2021Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Even though aging and cellular senescence appear to be linked, the biological mechanisms interconnecting these two processes remain to be unravelled. Therefore, microRNA (miRNA/miR) profiles were analyzed ex vivo by means of gene array in fibroblasts isolated from young and old human donors. Expression of several miRNAs was positively correlated with donor age. Among them, miR-23a-3p was shown to target hyaluronan synthase 2 (HAS2). HA is a polysaccharide of the extracellular matrix that critically regulates the phenotype of fibroblasts. Indeed, both aged and senescent fibroblasts showed increased miR-23a-3p expression and secreted significantly lower amounts of HA compared with young and non-senescent fibroblasts. Ectopic overexpression of miR-23a-3p in non-senescent fibroblasts led to decreased HAS2-mediated HA synthesis, upregulation of senescence-associated markers, and decreased proliferation. In addition, siRNA-mediated downregulation of HAS2 and pharmacological inhibition of HA synthesis by 4-methylumbelliferone mimicked the effects of miR-23a-3p. In vivo, miR-23a-3p was upregulated and HAS2 was downregulated in the skin of old mice compared with young mice. Inhibition of HA synthesis by 4-methylumbelliferone in mice reduced dermal hydration and viscoelasticity, thereby mimicking an aged skin phenotype. Taken together, these findings appear to link miR-23a-3p and the HA microenvironment as effector mechanisms in both dermal aging and senescence.
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.