ArticleAtherosclerosis2012
Lysophosphatidic acid causes endothelial dysfunction in porcine coronary arteries and human coronary artery endothelial cells.
Article in Atherosclerosis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
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
17 citing papers in PubMed, 28 citations in OpenAlex.
- Lysophosphatidylcholine and lysophosphatidic acid as key messengers in atherosclerosis: from a lipid-inflammation vicious cycle to therapeutic translation.Frontiers in cardiovascular medicine · 2026Review
- Metabolic alterations of endothelial cells under transient and persistent hypoxia: study using a 3D microvessels-on-chip model.Tissue barriers · 2025Article
- Autotaxin-Lysophosphatidate Axis: Promoter of Cancer Development and Possible Therapeutic Implications.International journal of molecular sciences · 2024Review
- Exploring the role of osteoglycin in type 2 diabetes: implications for insulin resistance and vascular pathophysiology.American journal of physiology. Endocrinology and metabolism · 2023Article
- The Long-Term Effects of Prenatal Hypoxia on Coronary Artery Function of the Male and Female Offspring.Biomedicines · 2022Article
- Disrupted Blood-Brain Barrier and Mitochondrial Impairment by Autotaxin-Lysophosphatidic Acid Axis in Postischemic Stroke.Journal of the American Heart Association · 2021Article
- Review
- Lysophosphatidic acid acts on LPABritish journal of pharmacology · 2018Article
- Lysophospholipids and Their Receptors Serve as Conditional DAMPs and DAMP Receptors in Tissue Oxidative and Inflammatory Injury.Antioxidants & redox signaling · 2018Article
- Review
- Secretory leukocyte protease inhibitor promising protective roles in obesity-associated atherosclerosis.Experimental biology and medicine (Maywood, N.J.) · 2017Review
- The phospholipase A2 activity of peroxiredoxin 6 modulates NADPH oxidase 2 activation via lysophosphatidic acid receptor signaling in the pulmonary endothelium and alveolar macrophages.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Small lipidated anti-obesity compounds derived from neuromedin U.European journal of medicinal chemistry · 2015Article
- Source and role of intestinally derived lysophosphatidic acid in dyslipidemia and atherosclerosis.Journal of lipid research · 2015Article
- Lysophosphatidic acid induces vasodilation mediated by LPA1 receptors, phospholipase C, and endothelial nitric oxide synthase.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Article
- Transgenic 6F tomatoes act on the small intestine to prevent systemic inflammation and dyslipidemia caused by Western diet and intestinally derived lysophosphatidic acid.Journal of lipid research · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
aimThe objective of this study was to determine the effects of lysophosphatidic acid (LPA) on endothelial functions and molecular alternations in both porcine coronary arteries and human coronary artery endothelial cells (HCAECs). METHODS AND
resultsThe vessel rings and HCAECs were treated with clinically relevant concentrations of LPA for different times. Vasomotor reactivity was studied with a myograph tension system. LPA (10 and 50 μM) treatment for the vessel rings significantly reduced endothelium-dependent vasorelaxation in response to bradykinin (×10(-5)M) by 32% and 49%, respectively, compared with the control (P<0.05). LPA decreased endothelial nitric oxide synthase (eNOS) mRNA and immunoreactivity levels in the vessel rings. In HCAECs, LPA reduced eNOS mRNA, phospho-eNOS and total eNOS protein levels. In addition, superoxide anion levels in LPA-treated vessel rings and HCAECs were significantly increased by lucegenin-enhanced chemiluminescence assay and dihydroethidium staining, respectively. Mitochondrial membrane potential and ATP content in LPA-treated HCAECs were substantially decreased. The mRNA levels of reactive oxygen species generating enzymes NOX4 and p40(phox) were increased, while endogenous antioxidant enzyme superoxide dismutase 1 was decreased in response to LPA treatment in HCAECs. Furthermore, exogenous antioxidant molecule selenomethionine (SeMet) effectively reversed these LPA-induced effects in both porcine coronary arteries and HCAECs.
conclusionsLPA causes endothelial dysfunction by a mechanism associated with decreased eNOS expression and increased oxidative stress in porcine coronary arteries and HCAECs.
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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.