ArticleOxidative medicine and cellular longevity2018
A Positive Feedback Loop of Profilin-1 and RhoA/ROCK1 Promotes Endothelial Dysfunction and Oxidative Stress.
Article in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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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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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
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Pulmonary hypertension secondary to congenital diaphragmatic hernia: factors and pathways involved in pulmonary vascular remodeling.Pediatric research · 2019Pooled it
- RAGE Axis in the Pathogenesis and Treatment of CNS Neurodegeneration in Long-Term Hyperglycemia.International journal of molecular sciences · 2026Review
- A Spatially Resolved View on the Aging Substantia nigra: An Exploratory Proteomic Study.Advanced biology · 2025Article
- Glucose Metabolism Reprogramming of Vascular Endothelial Cells and Its Implication in Development of Atherosclerosis.Reviews in cardiovascular medicine · 2024Review
- Comprehensive Assessment of Ischemic Stroke in Nonhuman Primates: Neuroimaging, Behavioral, and Serum Proteomic Analysis.ACS chemical neuroscience · 2024Article
- Identification and RT-qPCR Validation of Biomarkers Based on Butyrate Metabolism-Related Genes to Predict Recurrent Miscarriage.Journal of inflammation research · 2024Article
- Transcriptome analysis of the cerebral cortex of acrylamide-exposed wild-type and IL-1β-knockout mice.Archives of toxicology · 2024Article
- RhoA/ROCK1 regulates the mitochondrial dysfunction through Drp1 induced by Porphyromonas gingivalis in endothelial cells.Journal of cellular and molecular medicine · 2023Article
- Trophoblast Exosomal UCA1 Induces Endothelial Injury through the PFN1-RhoA/ROCK Pathway in Preeclampsia: A Human-Specific Adaptive Pathogenic Mechanism.Oxidative medicine and cellular longevity · 2022Article
- Profilin-1 is involved in macroangiopathy induced by advanced glycation end productsWorld journal of diabetes · 2021Article
- Review
- The role of profilin-1 in cardiovascular diseases.Journal of cell science · 2021Review
- Profilin: many facets of a small protein.Biophysical reviews · 2020Review
- Advanced glycosylation end products (AGEs) controls proliferation, invasion and permeability through orchestrating ARHGAP18/RhoA pathway in human umbilical vein endothelial cells.Glycoconjugate journal · 2020Article
- Protein Tyrosine Phosphatase Receptor S Acts as a Metastatic Suppressor in Malignant Peripheral Nerve Sheath Tumor via Profilin 1-Induced Epithelial-Mesenchymal Transition.Frontiers in cell and developmental biology · 2020Article
- Mechanisms of endothelial stiffening in dyslipidemia and aging: Oxidized lipids and shear stress.Current topics in membranes · 2020Review
- Rho and Reactive Oxygen Species at Crossroads of Endothelial Permeability and Inflammation.Antioxidants & redox signaling · 2019Article
- Building Blood Vessels-One Rho GTPase at a Time.Cells · 2019Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular endothelial dysfunction is considered critical development in the progression of cardiovascular events and is associated with vascular damage and oxidative stress. Previous studies have shown that profilin-1 could be induced by advanced glycation end products (AGEs) and contributes to vascular hyperpermeability; however, the mechanisms are not fully understood. In this study, we sought to assess whether reactive oxygen species (ROS) were involved in profilin-1-mediated RhoA/ROCK1 signaling. Treatment with AGEs significantly induced the expression of profilin-1 and ROS production in human umbilical vein endothelial cells (HUVECs), whereas knockdown of profilin-1 diminished AGE-induced RhoA and ROCK1 activation and ROS production. Moreover, ectopic overexpression of profilin-1 also increased RhoA and ROCK1 activation and ROS production under low AGE concentration. Furthermore, blockage of RhoA/ROCK1 with the inhibitors CT04 and Y27632 significantly attenuated the profilin-1-mediated cell damage and ROS production. Additionally, ROS inhibition resulted in a significant decrease in profilin-1-mediated RhoA/ROCK1 expression, suggesting that the regulation of RhoA/ROCK1 signaling was partly independent of ROS. Taken together, these results suggested that the RhoA/ROCK1 pathway activated by excessive ROS is responsible for profilin-1-mediated endothelial damage.
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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.