ArticleCell death & disease2014
MiR-216a: a link between endothelial dysfunction and autophagy.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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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.
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Who cites it
88 citing papers in PubMed, 144 citations in OpenAlex.
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- Enhancing Therapeutic Efficacy in Cancer Treatment: Integrating Nanomedicine with Autophagy Inhibition Strategies.ACS omega · 2024Review
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- Homocysteine metabolites inhibit autophagy by upregulating miR-21-5p, miR-155-5p, miR-216-5p, and miR-320c-3p in human vascular endothelial cells.Scientific reports · 2024Article
- Effect of reactive oxygen, nitrogen, and sulfur species on signaling pathways in atherosclerosis.Vascular pharmacology · 2024Review
- The SGLT2 inhibitor empagliflozin attenuates atherosclerosis progression by inducing autophagy.Journal of physiology and biochemistry · 2024Article
- High-density lipoprotein regulates angiogenesis by affecting autophagy via miRNA-181a-5p.Science China. Life sciences · 2024Article
- Analysis of extracellular vesicle microRNA profiles reveals distinct blood and lymphatic endothelial cell origins.Journal of extracellular biology · 2024Article
- Recent progress of endoplasmic reticulum stress in the mechanism of atherosclerosis.Frontiers in cardiovascular medicine · 2024Review
- Endothelial Cell Aging and Autophagy Dysregulation.Cardiovascular & hematological agents in medicinal chemistry · 2024Review
- Autophagy Behavior in Endothelial Cell Regeneration.Current aging science · 2024Review
- Ginsenoside Rb2 improves heart failure by down-regulating miR-216a-5p to promote autophagy and inhibit apoptosis and oxidative stress.Journal of applied biomedicine · 2023Article
- MicroRNA-216a is essential for cardiac angiogenesis.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Spermidine improves angiogenic capacity of senescent endothelial cells, and enhances ischemia-induced neovascularization in aged mice.Scientific reports · 2023Article
- Review
28 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial dysfunction and impaired autophagic activity have a crucial role in aging-related diseases such as cardiovascular dysfunction and atherosclerosis. We have identified miR-216a as a microRNA that is induced during endothelial aging and, according to the computational analysis, among its targets includes two autophagy-related genes, Beclin1 (BECN1) and ATG5. Therefore, we have evaluated the role of miR-216a as a molecular component involved in the loss of autophagic function during endothelial aging. The inverse correlation between miR-216a and autophagic genes was conserved during human umbilical vein endothelial cells (HUVECs) aging and in vivo models of human atherosclerosis and heart failure. Luciferase experiments indicated BECN1, but not ATG5 as a direct target of miR-216a. HUVECs were transfected in order to modulate miR-216a expression and stimulated with 100 μg/ml oxidized low-density lipoprotein (ox-LDL) to induce a stress repairing autophagic process. We found that in young HUVECs, miR-216a overexpression repressed BECN1 and ATG5 expression and the ox-LDL induced autophagy, as evaluated by microtubule-associated protein 1 light chain 3 (LC3B) analysis and cytofluorimetric assay. Moreover, miR-216a stimulated ox-LDL accumulation and monocyte adhesion in HUVECs. Conversely, inhibition of miR-216a in old HUVECs rescued the ability to induce a protective autophagy in response to ox-LDL stimulus. In conclusion, mir-216a controls ox-LDL induced autophagy in HUVECs by regulating intracellular levels of BECN1 and may have a relevant role in the pathogenesis of cardiovascular disorders and atherosclerosis.
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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.