ArticleOncotarget2016
MiR-23a-depressed autophagy is a participant in PUVA- and UVB-induced premature senescence.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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.
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Who cites it
28 citing papers in PubMed, 53 citations in OpenAlex.
- Advances in skin aging: integrating epigenetic, cellular, and immune mechanisms for targeted therapy.Immunity & ageing : I & A · 2026Review
- Prolonged Survival with Dieting for Improved Autophagy.Non-coding RNA · 2025Review
- miR-23a-mediated TRF2 repression in CD4 T cells from PLWH.Molecular immunology · 2025Article
- Dysregulation of autophagy during photoaging reduce oxidative stress and inflammatory damage caused by UV.Frontiers in pharmacology · 2025Review
- Role of non‑coding RNAs in UV‑induced radiation effects (Review).Experimental and therapeutic medicine · 2024Review
- Orchestrating Cellular Balance: ncRNAs and RNA Interactions at the Dominant of Autophagy Regulation in Cancer.International journal of molecular sciences · 2024Review
- Identification of lncRNA-miRNA-mRNA Regulatory Network and Therapeutic Agents for Skin Aging by Bioinformatics Analysis.Biochemical genetics · 2023Article
- MicroRNAs in Age-Related Proteostasis and Stress Responses.Non-coding RNA · 2023Review
- Non-coding RNAs in photoaging-related mechanisms: a new paradigm in skin health.Biogerontology · 2022Review
- Autophagy plays an essential role in ultraviolet radiation-driven skin photoaging.Frontiers in pharmacology · 2022Review
- HSP27 Protects Skin From Ultraviolet B -Induced Photodamage by Regulating Autophagy and Reactive Oxygen Species Production.Frontiers in cell and developmental biology · 2022Article
- Autophagy and the hallmarks of aging.Ageing research reviews · 2021Review
- Targeting microRNA for improved skin health.Health science reports · 2021Review
- Review
- The Sex-Related Interplay between TME and Cancer: On the Critical Role of Estrogen, MicroRNAs and Autophagy.Cancers · 2021Review
- Histological Evaluation and Gene Expression Profiling of Autophagy-Related Genes for Cartilage of Young and Senescent Rats.International journal of molecular sciences · 2020Article
- The Role of microRNAs in Organismal and Skin Aging.International journal of molecular sciences · 2020Review
- Hopes and Limits of Adipose-Derived Stem Cells (ADSCs) and Mesenchymal Stem Cells (MSCs) in Wound Healing.International journal of molecular sciences · 2020Review
- Cerebral Amyloid Angiopathy, Alzheimer's Disease and MicroRNA: miRNA as Diagnostic Biomarkers and Potential Therapeutic Targets.Neuromolecular medicine · 2019Review
- Interaction among inflammasome, autophagy and non-coding RNAs: new horizons for drug.Precision clinical medicine · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is a cellular catabolic mechanism that is activated in response to stress conditions, including ultraviolet (UV) irradiation, starvation, and misfolded protein accumulation. Abnormalities in autophagy are associated with several pathologies, including aging and cancer. Furthermore, recent studies have demonstrated that microRNAs (miRNAs) are potent modulators of the autophagy pathway. As a result, the current study aims to elucidate the role of the autophagy-related miRNA miR-23ain the process of photoaging. Experiments demonstrated that the antagomir-mediated inactivation of miR-23a resulted in the stimulation of PUVA- and UVB-depressed autophagy flux and protected human fibroblasts from premature senescence. Furthermore, AMBRA1 was identified as a miR-23a target. AMBRA1 cellular levels increased following the introduction of miR-23a antagomirs. And a bioinformatics analysis revealed that the AMBRA1 3' UTR contains functional miR-23a responsive sequences. Finally, it was also demonstrated that both AMBRA1 overexpression and Rapamycin treatment were both able to rescue fibroblasts from PUVA and UVB irradiation-induced autophagy inhibition, but that these effects could also be mitigated by miR-23a overexpression. Therefore, this study concludes that miR-23a-regulated autophagy is a novel and important regulator of ultraviolet-induced premature senescence and AMBRA1 is a rate-limiting miRNA target in this pathway.
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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.