ArticleAntioxidants & redox signaling2014
Hypoxia-induced miR-210 modulates tissue response to acute peripheral ischemia.
Article in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 51 citations in OpenAlex.
- Small Extracellular Vesicles in Cardioprotection, Cardiac Repair, and Regeneration: Cargo Mechanisms, Producer Cell Sources, and Translational Development.Biomedicines · 2026Review
- Article
- 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
- miR-210 overexpression increases pressure overload-induced cardiac fibrosis.Non-coding RNA research · 2025Article
- Non-coding RNAs and angiogenesis in cardiovascular diseases: a comprehensive review.Molecular and cellular biochemistry · 2024Review
- Implication of microRNAs as messengers of exercise adaptation in junior female triathlonists.Scientific reports · 2024Article
- Hypoxia-preconditioned WJ-MSC spheroid-derived exosomes delivering miR-210 for renal cell restoration in hypoxia-reoxygenation injury.Stem cell research & therapy · 2024Article
- Dysregulated Genes, MicroRNAs, Biological Pathways, and Gastrocnemius Muscle Fiber Types Associated With Progression of Peripheral Artery Disease: A Preliminary Analysis.Journal of the American Heart Association · 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
- Elevated level of microRNA-210 at the initiation of muscular regeneration in acetic acid-induced non-ischemic skeletal muscular injury in mice.Journal of toxicologic pathology · 2022Article
- Role of microRNAs in trophoblast invasion and spiral artery remodeling: Implications for preeclampsia.Frontiers in cell and developmental biology · 2022Review
- Downregulation of microRNA-185 expression in diabetic patients increases the expression of NOS2 and results in vascular injury.Experimental and therapeutic medicine · 2021Article
- Review
- Genetics of macrovascular complications in type 2 diabetes.World journal of diabetes · 2021Review
- Macrophage miR-210 induction and metabolic reprogramming in response to pathogen interaction boost life-threatening inflammation.Science advances · 2021Article
- Hypoxia-induced miR-210 modulates the inflammatory response and fibrosis upon acute ischemia.Cell death & disease · 2021Article
- The Role of Circulating Biomarkers in Peripheral Arterial Disease.International journal of molecular sciences · 2021Review
- Treatment of Oxidative Stress with Exosomes in Myocardial Ischemia.International journal of molecular sciences · 2021Review
- HypoxamiR-210 accelerates wound healing in diabetic mice by improving cellular metabolism.Communications biology · 2020Article
- MicroRNA-210 improves perfusion recovery following hindlimb ischemia via suppressing reactive oxygen species.Experimental and therapeutic medicine · 2020Article
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 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsPeripheral artery disease is caused by the restriction or occlusion of arteries supplying the leg. Better understanding of the molecular mechanisms underpinning tissue response to ischemia is urgently needed to improve therapeutic options. The aim of this study is to investigate hypoxia-induced miR-210 regulation and its role in a mouse model of hindlimb ischemia.
resultsmiR-210 expression was induced by femoral artery dissection. To study the role of miR-210, its function was inhibited by the systemic administration of a miR-210 complementary locked nucleic acid (LNA)-oligonucleotide (anti-miR-210). In the ischemic skeletal muscle, anti-miR-210 caused a marked decrease of miR-210 compared with LNA-scramble control, while miR-210 target expression increased accordingly. Histological evaluation of acute tissue damage showed that miR-210 inhibition increased both apoptosis at 1 day and necrosis at 3 days. Capillary density decrease caused by ischemia was significantly more pronounced in anti-miR-210-treated mice; residual limb perfusion decreased accordingly. To investigate the molecular mechanisms underpinning the increased damage triggered by miR-210 blockade, we tested the impact of anti-miR-210 treatment on the transcriptome. Gene expression analysis highlighted the deregulation of mitochondrial function and redox balance. Accordingly, oxidative damage was more severe in the ischemic limb of anti-miR-210-treated mice and miR-210 inhibition increased oxidative metabolism. Further, oxidative-stress resistant p66(Shc)-null mice displayed decreased tissue damage following ischemia. INNOVATION: This study identifies miR-210 as a crucial element in the adaptive mechanisms to acute peripheral ischemia.
conclusionsThe physiopathological significance of miR-210 is context dependent. In the ischemic skeletal muscle it seems to be cytoprotective, regulating oxidative metabolism and oxidative stress.
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.