ArticleFrontiers in cardiovascular medicine2021
p53 SUMOylation Mediates AOPP-Induced Endothelial Senescence and Apoptosis Evasion.
Article in Frontiers in cardiovascular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Engineering etiology-aligned in vitro models of human vessels.Microsystems & nanoengineering · 2026Review
- UBC9-mediated p53 SUMOylation drives tubular senescence and exacerbates acute kidney injury in mice.Acta pharmacologica Sinica · 2026Article
- Cardiovascular Risk and Its Presentation in Chronic Kidney Disease.Journal of clinical medicine · 2025Review
- AQP1 differentially orchestrates endothelial cell senescence.Redox biology · 2024Article
- Post-translational modifications in kidney diseases and associated cardiovascular risk.Nature reviews. Nephrology · 2024Review
- Review
- Quantitative Assessment of Intracellular Effectors and Cellular Response in RAGE Activation.Archives of internal medicine research · 2024Article
- Implications of receptor for advanced glycation end products for progression from obesity to diabetes and from diabetes to cancer.World journal of diabetes · 2023Review
- Endothelial senescence in vascular diseases: current understanding and future opportunities in senotherapeutics.Experimental & molecular medicine · 2023Review
- Cardiac-targeted PIASy gene silencing mediates deSUMOylation of caveolin-3 and prevents ischemia/reperfusion-induced NaMilitary Medical Research · 2022Article
- A potential role of autophagy-mediated vascular senescence in the pathophysiology of HFpEF.Frontiers in endocrinology · 2022Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aging of endothelial cells plays a critical role in the development of age-related vascular disease. We established a model of endothelial premature senescence by application of Advanced oxidation protein products (AOPPs) modified bovine serum albumin (AOPP-BSA) in human umbilical vein endothelial cells (HUVECs). This cellular senescence was accompanied with endothelial barrier dysfunction and angiogenesis impairment. It was further revealed that these senescent HUVECs underwent apoptosis evasion and the receptor for advanced glycation endproducts (RAGE) played a role in these processes. The AOPP-induced senescence was regulated by the state of autophagy in HUVECs. We further proved that AOPP-BSA attenuated the autophagy of HUVECs, led to p53 SUMOylation at K386, resulting in endothelial senescence. We also established the animal model of vascular senescence by using ApoE
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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.