ArticlePloS one2014
eNOS-dependent antisenscence effect of a calcium channel blocker in human endothelial cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 34 citations in OpenAlex.
- Pharmacotherapeutic Considerations on Telomere Biology: The Positive Effect of Pharmacologically Active Substances on Telomere Length.International journal of molecular sciences · 2024Review
- The role of telomerase reverse transcriptase in the mitochondrial protective functions of Angiotensin-(1-7) in diabetic CD34Biochemical pharmacology · 2024Article
- The long and the short of it: Salivary telomere length as a candidate biomarker for hypertension and age-related changes in blood pressure.Physiological reports · 2024Article
- Hypertension and cellular senescence.Biogerontology · 2023Review
- Review
- Effects of different enantiomers of amlodipine on lipid profiles and vasomotor factors in atherosclerotic rabbits.Open life sciences · 2021Article
- Role of the Scavenger Receptor CD36 in Accelerated Diabetic Atherosclerosis.International journal of molecular sciences · 2020Article
- Longitudinal Association of Telomere Attrition with the Effects of Antihypertensive Treatment and Blood Pressure Lowering.Aging and disease · 2020Article
- Pretreatment with cilnidipine attenuates hypoxia/reoxygenation injury in HL-1 cardiomyocytes through enhanced NO production and action potential shortening.Hypertension research : official journal of the Japanese Society of Hypertension · 2020Article
- Verapamil extends lifespan inAging · 2020Article
- Roles of eNOS in atherosclerosis treatment.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019Review
- Resveratrol attenuates high glucose-induced endothelial cell apoptosis via mediation of store-operated calcium entry.Molecular and cellular biochemistry · 2018Article
- Administration of L-arginine plus L-citrulline or L-citrulline alone successfully retarded endothelial senescence.PloS one · 2018Article
- Membrane ion Channels and Receptors in Animal lifespan Modulation.Journal of cellular physiology · 2017Review
- Blood pressure normalization via pharmacotherapy improves cutaneous microvascular function through NO-dependent and NO-independent mechanisms.Microcirculation (New York, N.Y. : 1994) · 2017Article
- Implications of telomeres and telomerase in endometrial pathology.Human reproduction update · 2017Review
- Nitric oxide, interorganelle communication, and energy flow: a novel route to slow aging.Frontiers in cell and developmental biology · 2015Review
- Article
- Role of the Pancreatic Islet Microvasculature in Health and Disease.The journal of histochemistry and cytochemistry : official journal of the Histochemistry SocietyReview
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Senescence of vascular endothelial cells is an important contributor to the pathogenesis of age-associated vascular disorders such as atherosclerosis. We investigated the effects of antihypertensive agents on high glucose-induced cellular senescence in human umbilical venous endothelial cells (HUVECs). Exposure of HUVECs to high glucose (22 mM) for 3 days increased senescence-associated- β-galactosidase (SA-β-gal) activity, a senescence marker, and decreased telomerase activity, a replicative senescence marker. The calcium channel blocker nifedipine, but not the β1-adrenergic blocking agent atenolol or the angiotensin-converting enzyme inhibitor perindopril, reduced SA-β-gal positive cells and prevented a decrease in telomerase activity in a high-glucose environment. This beneficial effect of nifedipine was associated with reduced reactive oxygen species (ROS) and increased endothelial nitric oxide synthase (eNOS) activity. Thus, nifedipine prevented high glucose-induced ROS generation and increased basal eNOS phosphorylation level at Ser-1177. Treatment with N (G)-nitro-L-arginine (L-NAME) and transfection of small interfering RNA (siRNA) targeting eNOS eliminated the anti-senscence effect of nifedipine. These results demonstrate that nifedipine can prevent endothelial cell senescence in an eNOS-dependent manner. The anti-senescence action of nifedipine may represent a novel mechanism by which it protects against atherosclerosis.
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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.