ArticleCardiovascular research2011
Membrane raft-lysosome redox signalling platforms in coronary endothelial dysfunction induced by adipokine visfatin.
Article in Cardiovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 64 citations in OpenAlex.
- Acid Sphingomyelinase and Ceramide Signaling Pathway Mediates Nicotine-Induced NLRP3 Inflammasome Activation and Podocyte Injury.Biomedicines · 2025Article
- Integrative analysis of single-cell RNA-seq and gut microbiome metabarcoding data elucidates macrophage dysfunction in mice with DSS-induced ulcerative colitis.Communications biology · 2024Article
- Regulation of NLRP3 Inflammasome Activation and Inflammatory Exosome Release in Podocytes by Acid Sphingomyelinase During Obesity.Inflammation · 2023Article
- Regulation of TRPML1 channel activity and inflammatory exosome release by endogenously produced reactive oxygen species in mouse podocytes.Redox biology · 2021Article
- Lysosome Function in Cardiovascular Diseases.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2021Review
- Hyperbaric oxygen activates visfatin expression and angiogenesis via angiotensin II and JNK pathway in hypoxic human coronary artery endothelial cells.Journal of cellular and molecular medicine · 2020Article
- Inhibitory effects of growth differentiation factor 11 on autophagy deficiency-induced dedifferentiation of arterial smooth muscle cells.American journal of physiology. Heart and circulatory physiology · 2019Article
- Podocyte NLRP3 Inflammasome Activation and Formation by Adipokine Visfatin.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2019Article
- Protective Role of Autophagy in Nlrp3 Inflammasome Activation and Medial Thickening of Mouse Coronary Arteries.The American journal of pathology · 2018Article
- Targeted and Off-Target (Bystander and Abscopal) Effects of Radiation Therapy: Redox Mechanisms and Risk/Benefit Analysis.Antioxidants & redox signaling · 2018Review
- Differential effects of short chain fatty acids on endothelial Nlrp3 inflammasome activation and neointima formation: Antioxidant action of butyrate.Redox biology · 2018Article
- Electron Paramagnetic Resonance Measurements of Reactive Oxygen Species by Cyclic Hydroxylamine Spin Probes.Antioxidants & redox signaling · 2018Review
- Endothelial NLRP3 inflammasome activation and arterial neointima formation associated with acid sphingomyelinase during hypercholesterolemia.Redox biology · 2017Article
- The tumor suppressor capability of p53 is dependent on non-muscle myosin IIA function in head and neck cancer.Oncotarget · 2017Article
- Sphingolipids in obesity and related complications.Frontiers in bioscience (Landmark edition) · 2017Review
- Contribution of p62 to Phenotype Transition of Coronary Arterial Myocytes with Defective Autophagy.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2017Article
- Implication of CD38 gene in autophagic degradation of collagen I in mouse coronary arterial myocytes.Frontiers in bioscience (Landmark edition) · 2017Article
- Interaction of hyperlipidemia and reactive oxygen species: Insights from the lipid-raft platform.World journal of cardiology · 2016Article
- Insights into the molecular mechanisms of diabetes-induced endothelial dysfunction: focus on oxidative stress and endothelial progenitor cells.Endocrine · 2015Article
- Instigation of endothelial Nlrp3 inflammasome by adipokine visfatin promotes inter-endothelial junction disruption: role of HMGB1.Journal of cellular and molecular medicine · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
aimsThe adipokine visfatin, produced during obesity, has been reported to participate in the development of cardiovascular disease associated with metabolic syndrome. The present study was designed to test a hypothesis that visfatin causes coronary endothelial dysfunction through lysosome trafficking and fusion to cell membranes, membrane raft (MR) clustering, and formation of redox signalosomes. METHODS AND
resultsBy using confocal microscopy, it was found that visfatin, but not adiponectin, stimulated NADPH oxidase (NOX) subunits, gp91(phox) aggregation in MR clusters and p47(phox) translocation to these MR clusters in bovine coronary arterial endothelial cells (CAECs), leading to activation of NOX with a 2.5-fold increase in O(2)(·-) production. A signalling lipid, ceramide, was found to be enriched in such membrane MR-NOX complexes of CAECs. Lysosomal fluorescent dye (FM1-43) quenching and de-quenching revealed that visfatin induced the fusion of lysosomes to cell membranes and incorporation of acid sphingomyelinase and its product, ceramide, in such MR-NOX signalling platforms. Functionally, visfatin significantly attenuated endothelium-dependent vasodilation in small coronary arteries (by 80%), which was blocked by lysosomal function inhibitor and MR disruptors.
conclusionThese results suggest that lysosome-associated molecular trafficking and consequent ceramide accumulation in cell membrane may mediate the assembly of NOX subunits and their activation in response to adipokine visfatin in CAECs, thereby producing endothelial dysfunction in coronary circulation.
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.