ArticleThe Journal of biological chemistry2010
Activation of AMP-activated protein kinase alpha1 alleviates endothelial cell apoptosis by increasing the expression of anti-apoptotic proteins Bcl-2 and survivin.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 45 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
45 citing papers in PubMed, 83 citations in OpenAlex.
- Metformin alleviates neurocognitive impairment in aging via activation of AMPK/BDNF/PI3K pathway.Scientific reports · 2022Article
- Role of AMPK in Myocardial Ischemia-Reperfusion Injury-Induced Cell Death in the Presence and Absence of Diabetes.Oxidative medicine and cellular longevity · 2022Review
- Overexpression of long non-coding RNA ANRIL promotes post-ischaemic angiogenesis and improves cardiac functions by targeting Akt.Journal of cellular and molecular medicine · 2020Article
- Avenanthramide-C Restores Impaired Plasticity and Cognition in Alzheimer's Disease Model Mice.Molecular neurobiology · 2020Article
- Cancer therapeutics using survivin BIRC5 as a target: what can we do after over two decades of study?Journal of experimental & clinical cancer research : CR · 2019Review
- Myeloid-Specific Deletion of the AMPKα2 Subunit Alters Monocyte Protein Expression and Atherogenesis.International journal of molecular sciences · 2019Article
- Inhibition of miRNA-27b enhances neurogenesis via AMPK activation in a mouse ischemic stroke model.FEBS open bio · 2019Article
- Celecoxib exerts protective effects in the vascular endothelium via COX-2-independent activation of AMPK-CREB-Nrf2 signalling.Scientific reports · 2018Article
- Sodium salicylate modulates inflammatory responses through AMP-activated protein kinase activation in LPS-stimulated THP-1 cells.Journal of cellular biochemistry · 2018Article
- Flow signaling and atherosclerosis.Cellular and molecular life sciences : CMLS · 2017Review
- How AMPK and PKA Interplay to Regulate Mitochondrial Function and Survival in Models of Ischemia and Diabetes.Oxidative medicine and cellular longevity · 2017Review
- Adiponectin enhances bone marrow mesenchymal stem cell resistance to flow shear stress through AMP-activated protein kinase signaling.Scientific reports · 2016Article
- Activation of hERG3 channel stimulates autophagy and promotes cellular senescence in melanoma.Oncotarget · 2016Article
- Macrophage-epithelial paracrine crosstalk inhibits lung edema clearance during influenza infection.The Journal of clinical investigation · 2016Article
- Methotrexate-mediated activation of an AMPK-CREB-dependent pathway: a novel mechanism for vascular protection in chronic systemic inflammation.Annals of the rheumatic diseases · 2016Article
- Effects of metformin treatment on glioma-induced brain edema.American journal of translational research · 2016Article
- Cellular and molecular biology of aging endothelial cells.Journal of molecular and cellular cardiology · 2015Review
- The twisted survivin connection to angiogenesis.Molecular cancer · 2015Review
- Shear stress-induced mitochondrial biogenesis decreases the release of microparticles from endothelial cells.American journal of physiology. Heart and circulatory physiology · 2015Article
- AICAR attenuates organ injury and inflammatory response after intestinal ischemia and reperfusion.Molecular medicine (Cambridge, Mass.) · 2015Article
Corrections and comments
- Retraction · 2020-01-10Duplication of/in Image · Error in Image · Objections by Author(s) · Upgrade/Update of Prior Notice(s) ·
- Expression of concern · 2019-06-21Concerns/Issues about Data · Concerns/Issues about Results and/or Conclusions · Updated to Retraction ·
- Expression of concern
- Retracted
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Accumulating evidence suggests that AMP-activated protein kinase (AMPK) activation exerts anti-apoptotic effects in multiple types of cells. However, the underlying mechanisms remain poorly defined. The aim of the present study was to determine how AMPK suppresses apoptosis in endothelial cells exposed to hypoxia and glucose deprivation (OGD). AMPK activity, NF-kappaB activation, and endothelial cell apoptosis were assayed in cultured endothelial cells and mouse common carotid artery with or without OGD treatment. OGD markedly activated AMPK as early as 30 min, and AMPK activity reached maximal at 2 h of OGD. Endothelial apoptosis was not detected until 2 h of OGD but became markedly elevated at 6 h of OGD treatment. Furthermore, AMPK inhibition by Compound C or overexpression of dominant negative AMPK (AMPK-DN) exacerbated, whereas AMPK activation by pharmacologic (aminoimidazole carboxamide ribonucleotide (AICAR)) or genetic means (overexpression of constitutively active AMPK) suppressed endothelial cell apoptosis caused by OGD. Concomitantly, AMPK activation increased the expression of both Bcl-2 and Survivin, two potent anti-apoptotic proteins. Furthermore, AMPK activation significantly enhanced IkappaBalpha kinase activation, NF-kappaB nuclear translocation, and DNA binding activity of NF-kappaB. Consistently, selective inhibition of NF-kappaB, which abolished OGD-enhanced expression of Bcl-2 and Survivin, accentuated endothelial apoptosis caused by OGD. Finally, we found that genetic deletion of the AMPKalpha1, but not AMPKalpha2, suppressed OGD-enhanced NF-kappaB activation, the expression of Bcl-2 and Survivin, and endothelial apoptosis. Overall, our results suggest that AMPKalpha1, but not AMPKalpha2 activation, promotes cell survival by increasing NF-kappaB-mediated expression of anti-apoptotic proteins (Bcl-2 and Survivin) and intracellular ATP contents.
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.