ArticlePloS one2012
Tyrosine nitration of PA700 links proteasome activation to endothelial dysfunction in mouse models with cardiovascular risk factors.
Article in PloS one, 2012. 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 It has been retracted, and should not be counted.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 17 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
17 citing papers in PubMed, 36 citations in OpenAlex.
- AiScience · 2023Article
- Article
- Oxidative Stress-Related Susceptibility to Aneurysm in Marfan's Syndrome.Biomedicines · 2021Review
- Build-UPS and break-downs: metabolism impacts on proteostasis and aging.Cell death and differentiation · 2021Review
- Proteasome Biology: Chemistry and Bioengineering Insights.Polymers · 2020Review
- Lovastatin upregulates microRNA-29b to reduce oxidative stress in rats with multiple cardiovascular risk factors.Oncotarget · 2017Article
- Priming the proteasome by protein kinase G: a novel cardioprotective mechanism of sildenafil.Future cardiology · 2015Review
- Redox regulation of endothelial cell fate.Cellular and molecular life sciences : CMLS · 2014Article
- Impaired proteostasis: role in the pathogenesis of diabetes mellitus.Diabetologia · 2014Review
- Regulation of cardiac proteasomes by ubiquitination, SUMOylation, and beyond.Journal of molecular and cellular cardiology · 2014Review
- RETRACTED: Identification of nitric oxide as an endogenous inhibitor of 26S proteasomes in vascular endothelial cells.PloS one · 2014Article
- Endothelial arginine resynthesis contributes to the maintenance of vasomotor function in male diabetic mice.PloS one · 2014Article
- Analysis of oxidative stress enzymes and structural and functional proteins on human aortic tissue from different aortopathies.Oxidative medicine and cellular longevity · 2014Article
- Coronary endothelial dysfunction and mitochondrial reactive oxygen species in type 2 diabetic mice.American journal of physiology. Cell physiology · 2013Article
- Therapeutic effect of MG132 on the aortic oxidative damage and inflammatory response in OVE26 type 1 diabetic mice.Oxidative medicine and cellular longevity · 2013Article
- Preventive and therapeutic effects of MG132 by activating Nrf2-ARE signaling pathway on oxidative stress-induced cardiovascular and renal injury.Oxidative medicine and cellular longevity · 2013Review
- Regulation of the proteasome by AMPK in endothelial cells: the role of O-GlcNAc transferase (OGT).PloS one · 2012Article
Corrections and comments
- Retraction · 2023-05-18Concerns/Issues about Data · Concerns/Issues about Image · Duplication of/in Image · Error in Image · Unreliable Data ·
- Retracted
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Oxidative stress is believed to cause endothelial dysfunction, an early event and a hallmark in cardiovascular diseases (CVD) including hypertension, diabetes, and dyslipidemia. However, the targets for oxidative stress-mediated endothelial dysfunction in CVD have not been completely elucidated. Here we report that 26S proteasome activation by peroxynitrite (ONOO(-)) is a common pathway for endothelial dysfunction in mouse models of diabetes, hypertension, and dyslipidemia. Endothelial function, assayed by acetylcholine-induced vasorelaxation, was impaired in parallel with significantly increased 26S proteasome activity in aortic homogenates from streptozotocin (STZ)-induced type I diabetic mice, angiotensin-infused hypertensive mice, and high fat-diets-fed LDL receptor knockout (LDLr(-/-)) mice. The elevated 26S proteasome activities were accompanied by ONOO(-)-mediated PA700/S10B nitration and increased 26S proteasome assembly and caused accelerated degradation of molecules (such as GTPCH I and thioredoxin) essential to endothelial homeostasis. Pharmacological (administration of MG132) or genetic inhibition (siRNA knockdown of PA700/S10B) of the 26S proteasome blocked the degradation of the vascular protective molecules and ablated endothelial dysfunction induced by diabetes, hypertension, and western diet feeding. Taken together, these results suggest that 26S proteasome activation by ONOO(-)-induced PA700/S10B tyrosine nitration is a common route for endothelial dysfunction seen in mouse models of hypertension, diabetes, and dyslipidemia.
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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.