ReviewCardiovascular research2011
Nitric oxide: a key factor behind the dysfunctionality of endothelial progenitor cells in diabetes mellitus type-2.
Review in Cardiovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03398356 (The Assessment of the Effect of Metformin and Its Serum Concentration on the Concentration of Substances Associated With the Production of Nitric Oxide in Patients With Impaired Carbohydrate Metabolism), which is not on this map. Cited by 34 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.
The Assessment of the Effect of Metformin and Its Serum Concentration on the Concentration of Substances Associated With the Production of Nitric Oxide in Patients With Impaired Carbohydrate Metabolism
Who cites it
34 citing papers in PubMed, 116 citations in OpenAlex.
- Single-cell chromatin accessibility landscape of cardiac non-myocytes identifies tissue repair program during heart regeneration.NPJ Regenerative medicine · 2026Article
- Sodium Butyrate, A Gut Microbiota Derived Metabolite in Type 2 Diabetes Mellitus and Cardiovascular Disease: A Review.Cardiovascular & hematological agents in medicinal chemistry · 2025Review
- Endothelial progenitor cells for diabetic cardiac and kidney disease.Stem cells translational medicine · 2024Review
- Mitochondria targeted esculetin administration improves insulin resistance and hyperglycemia-induced atherosclerosis in db/db mice.Journal of molecular medicine (Berlin, Germany) · 2024Article
- CXCR7 Agonist TC14012 Improves Angiogenic Function of Endothelial Progenitor Cells via Activating Akt/eNOS Pathway and Promotes Ischemic Angiogenesis in Diabetic Limb Ischemia.Cardiovascular drugs and therapy · 2023Article
- Effects of sesame (Food science & nutrition · 2023Review
- Article
- Overexpression of E3 ubiquitin ligase Cbl attenuates endothelial dysfunction in diabetes mellitus by inhibiting the JAK2/STAT4 signaling and Runx3-mediated H3K4me3.Journal of translational medicine · 2021Article
- HuR/Cx40 downregulation causes coronary microvascular dysfunction in type 2 diabetes.JCI insight · 2021Article
- Long Term Response to Circulating Angiogenic Cells, Unstimulated or Atherosclerotic Pre-Conditioned, in Critical Limb Ischemic Mice.Biomedicines · 2021Article
- Differences in the reaction of hyperlipidemia on different endothelial progenitor cells based on sex.Biomedical reports · 2021Article
- Higher levels of daily physical activity are associated with better skin microvascular function in type 2 diabetes-The Maastricht Study.Microcirculation (New York, N.Y. : 1994) · 2020Observational
- Icariin reduces high glucose-induced endothelial progenitor cell dysfunction via inhibiting the p38/CREB pathway and activating the Akt/eNOS/NO pathway.Experimental and therapeutic medicine · 2019Article
- Anti-PCSK9 antibodies inhibit pro-atherogenic mechanisms in APOE*3Leiden.CETP mice.Scientific reports · 2019Article
- Glyoxalase 1 Prevents Chronic Hyperglycemia Induced Heart-Explant Derived Cell Dysfunction.Theranostics · 2019Article
- Matrix-entrapped cellular secretome rescues diabetes-induced EPC dysfunction and accelerates wound healing in diabetic mice.PloS one · 2018Article
- There Is No Impact of Diabetes on the Endothelial Function of Chronic Kidney Disease Patients.Journal of diabetes research · 2018Article
- The role of epigenetics in renal ageing.Nature reviews. Nephrology · 2017Review
- Role of NADPH Oxidase-4 in Human Endothelial Progenitor Cells.Frontiers in physiology · 2017Article
- Molecular mechanisms associated with diabetic endothelial-erectile dysfunction.Nature reviews. Urology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes mellitus type-2 (DM-2) contributes to atherogenesis by inducing endothelial cell injury and dysfunction. Endothelial progenitor cells (EPCs) are essential to blood vessel formation, can differentiate into mature endothelial cells, and promote the repair of damaged endothelium. In DM-2, the circulating EPC count is low and their functionality is impaired. The mechanisms that underlie this reduced count and impaired functionality are poorly understood. Nitric oxide (NO) is a short-lived signalling molecule that is produced by vascular endothelial cells and participates in the maintenance of vascular tone. NO is also known to participate in other physiological processes, such as cell survival, proliferation, and migration. The bioavailability of NO is reduced in EPCs from DM-2 patients. Interestingly, an inverse relationship exists between the reduction in NO bioavailability in EPCs and the patient's plasma glucose and glycated haemoglobin levels. In addition, NO bioavailability in EPCs correlates with plasma oxidized low-density lipoprotein levels in DM-2. Although this reduction in NO bioavailability could be attributed to oxidative stress in DM-2 patients, it also may be due to impairment of one or more members of the protein signalling cascades that are responsible for NO production. The stimulation of NO production or its signalling cascades in EPCs may increase their numbers and improve their function, thus attenuating endothelium damage, independent of the vasodilatory effects of NO. This review summarizes the metabolic alterations that underlie the molecular mechanisms that may be responsible for EPC decrease and dysfunction in DM-2 with emphasis on the involvement of the NO system.
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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 Socratic graph.