ArticleDiabetes2015
miR-92a Corrects CD34+ Cell Dysfunction in Diabetes by Modulating Core Circadian Genes Involved in Progenitor Differentiation.
Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- 3D-Printable and Bioelectronic-Compatible Graphene-Reinforced PLA Nanocomposites Rejuvenate Aged Bone Regeneration Through Glycolytic Reprogramming.Advanced healthcare materials · 2026Article
- The role of hydroxyurea in modulating miRNA expression in sickle cell disease: molecular mechanisms and therapeutic implications.Annals of hematology · 2026Review
- Precision Medicine for Diabetic Retinopathy: Integrating Genetics, Biomarkers, Lifestyle, and AI.Genes · 2025Review
- Cohort-specific boolean models highlight different regulatory modules during Parkinson's disease progression.iScience · 2024Article
- Transcriptomic Profile of LinBMC genomics · 2024Article
- Holistic expression of miR-17-92 cluster in obesity, kidney diseases, cardiovascular diseases, and diabetes.Molecular biology reports · 2023Review
- Cardiovascular complications of diabetes: role of non-coding RNAs in the crosstalk between immune and cardiovascular systems.Cardiovascular diabetology · 2023Review
- Loss of CRY2 promotes regenerative myogenesis by enhancing PAX7 expression and satellite cell proliferation.MedComm · 2023Article
- miR-92a and integrin expression in fibrovascular membranes in proliferative diabetic retinopathy.Frontiers in ophthalmology · 2023Article
- The role of microRNAs in the molecular link between circadian rhythm and autism spectrum disorder.Animal cells and systems · 2023Review
- Lipids, hyperreflective crystalline deposits and diabetic retinopathy: potential systemic and retinal-specific effect of lipid-lowering therapies.Diabetologia · 2022Review
- Hypermethylation of miRNA-17-92 cluster in peripheral blood mononuclear cells in diabetic retinopathy.Diabetes & metabolic syndrome · 2022Article
- Pulmonary MicroRNA Changes Alter Angiogenesis in Chronic Obstructive Pulmonary Disease and Lung Cancer.Biomedicines · 2021Article
- RNA therapeutics for retinal diseases.Expert opinion on biological therapy · 2021Review
- MicroRNAs, Parkinson's Disease, and Diabetes Mellitus.International journal of molecular sciences · 2021Review
- Article
- MicroRNA, Diabetes Mellitus and Colorectal Cancer.Biomedicines · 2020Review
- MiR-92a regulates endothelial progenitor cells (EPCs) by targeting GDF11 via activate SMAD2/3/FAK/Akt/eNOS pathway.Annals of translational medicine · 2019Article
- Beneficial Effects of Angiotensin-(1-7) on CD34+ Cells From Patients With Heart Failure.Journal of cardiovascular pharmacology · 2018Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Autologous CD34(+) cells are widely used for vascular repair; however, in individuals with diabetes and microvascular disease these cells are dysfunctional. In this study, we examine expression of the clock genes Clock, Bmal, Per1, Per2, Cry1, and Cry2 in CD34(+) cells of diabetic and nondiabetic origin and determine the small encoding RNA (miRNA) profile of these cells. The degree of diabetic retinopathy (DR) was assessed. As CD34(+) cells acquired mature endothelial markers, they exhibit robust oscillations of clock genes. siRNA treatment of CD34(+) cells revealed Per2 as the only clock gene necessary to maintain the undifferentiated state of CD34(+) cells. Twenty-five miRNAs targeting clock genes were identified. Three of the miRNAs (miR-18b, miR-16, and miR-34c) were found only in diabetic progenitors. The expression of the Per2-regulatory miRNA, miR-92a, was markedly reduced in CD34(+) cells from individuals with DR compared with control subjects and patients with diabetes with no DR. Restoration of miR-92a levels in CD34(+) cells from patients with diabetes with DR reduced the inflammatory phenotype of these cells and the diabetes-induced propensity toward myeloid differentiation. Our studies suggest that restoring levels of miR-92a could enhance the usefulness of CD34(+) cells in autologous cell therapy.
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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.