ArticleScientific reports2017
Overexpression of miR-210 and its significance in ischemic tissue damage.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 52 citations in OpenAlex.
- Molecular Insights into the Regulatory Mechanisms Mediated by Hypoxia-Conditioned Skeletal Muscle Exosomal miRNAs.Biomarker insights · 2026Article
- Exploring the Vertical Transmission of Exosomes in Diagnostic and Therapeutic Targets for Pregnancy Complications.ACS biomaterials science & engineering · 2025Review
- Plasma microRNA-210 is associated with VEGF-A and EphrinA3 and relates to coronary collateral circulation in patients with coronary heart disease: a cross-sectional study.BMC cardiovascular disorders · 2025Article
- Differentially expressed ncRNAs as key regulators in infection of human bronchial epithelial cells by the SARS-CoV-2 Delta variant.Molecular therapy. Nucleic acids · 2025Article
- Current updates regarding biogenesis, functions and dysregulation of microRNAs in cancer: Innovative approaches for detection using CRISPR/Cas13‑based platforms (Review).International journal of molecular medicine · 2025Review
- miR-210 overexpression increases pressure overload-induced cardiac fibrosis.Non-coding RNA research · 2025Article
- Evaluation of miRNA-210 as a Prognostic Biomarker for Pre-eclampsia: A Case-Control Study.Cureus · 2025Article
- miR-210 is essential to retinal homeostasis in fruit flies and mice.Biology direct · 2024Article
- miR-210 in ischaemic stroke: biomarker potential, challenges and future perspectives.European journal of medical research · 2024Review
- MicroRNAs' Role in Diagnosis and Treatment of Subarachnoid Hemorrhage.Diseases (Basel, Switzerland) · 2023Review
- Exosomes derived from mesenchymal stem cells overexpressing miR-210 inhibits neuronal inflammation and contribute to neurite outgrowth through modulating microglia polarization.Open medicine (Warsaw, Poland) · 2023Article
- The role of miRNA-210 in pre-eclampsia development.Annals of medicine · 2022Review
- GSK3β Inhibition Is the Molecular Pivot That Underlies the Mir-210-Induced Attenuation of Intrinsic Apoptosis Cascade during Hypoxia.International journal of molecular sciences · 2022Article
- Skeletal muscle MiR-210 expression is associated with mitochondrial function in peripheral artery disease patients.Translational research : the journal of laboratory and clinical medicine · 2022Article
- Eph signaling is regulated by miRNA-210: Implications for corneal epithelial repair.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Electro-acupuncture Promotes Angiogenesis via Exosomal miR-210 in the Hypoxia-induced HUVECs Mediated HIF-1α/VEGF/Notch 1 Signal Pathway.Current neurovascular research · 2022Article
- Diagnostic and Prognostic Value of Dysregulated miR-10a-3p in Patients with Severe Pneumonia.Journal of inflammation research · 2022Article
- miR-210 Regulates Apoptotic Cell Death during Cellular Hypoxia and Reoxygenation in a Diametrically Opposite Manner.Biomedicines · 2021Article
- The lower expression of circulating miR-210 and elevated serum levels of HIF-1α in ischemic stroke; Possible markers for diagnosis and disease prediction.Journal of clinical laboratory analysis · 2021Article
- Genetics of macrovascular complications in type 2 diabetes.World journal of diabetes · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxia-induced miR-210 displays a pro-survival, cytoprotective and pro-angiogenic role in several in vitro systems. In vivo, we previously found that miR-210 inhibition increases ischemic damage. Here we describe the generation of a versatile transgenic mouse model allowing the evaluation of miR-210 therapeutic potential in ischemic cardiovascular diseases. We generated a Tet-On miR-210 transgenic mouse strain (TG-210) by targeted transgenesis in the ROSA26 locus. To functionally validate miR-210 transgenic mice, hindlimb ischemia was induced by femoral artery dissection. Blood perfusion was evaluated by power Doppler while tissue damage and inflammation were assessed by histological evaluation. We found that miR-210 levels were rapidly increased in TG-210 mice upon doxycycline administration. miR-210 overexpression was maintained over time and remained within physiological levels in multiple tissues. When hindlimb ischemia was induced, miR-210 overexpression protected from both muscular and vascular ischemic damage, decreased inflammatory cells density and allowed to maintain a better calf perfusion. In conclusion, we generated and functionally validated a miR-210 transgenic mouse model. Albeit validated in the context of a specific cardiovascular ischemic disease, miR-210 transgenic mice may also represent a useful model to assess the function of miR-210 in other physio-pathological conditions.
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.