ArticleCirculation research2009
Aldose reductase protects against early atherosclerotic lesion formation in apolipoprotein E-null mice.
Article in Circulation research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 73 citations in OpenAlex.
- Metabolic pathways for removing reactive aldehydes are diminished in the skeletal muscle during heart failure.Skeletal muscle · 2024Article
- Metabolic Pathways for Removing Reactive Aldehydes are Diminished in Atrophic Muscle During Heart Failure.Research square · 2023Article
- Article
- Effect of vinyl chloride exposure on cardiometabolic toxicity.Environmental toxicology · 2022Article
- Physiological and Pathological Roles of Aldose Reductase.Metabolites · 2021Review
- Aldose Reductase: An Emerging Target for Development of Interventions for Diabetic Cardiovascular Complications.Frontiers in endocrinology · 2021Review
- Exercise alters and β-alanine combined with exercise augments histidyl dipeptide levels and scavenges lipid peroxidation products in human skeletal muscle.Journal of applied physiology (Bethesda, Md. : 1985) · 2018Article
- Deficiency of aldose reductase exacerbates early pressure overload-induced cardiac dysfunction and autophagy in mice.Journal of molecular and cellular cardiology · 2018Article
- Biomarkers of Chronic Acrolein Inhalation Exposure in Mice: Implications for Tobacco Product-Induced Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- Atherogenesis and metabolic dysregulation in LDL receptor-knockout rats.JCI insight · 2017Article
- Aldose reductase (AKR1B) deficiency promotes phagocytosis in bone marrow derived mouse macrophages.Chemico-biological interactions · 2017Article
- Measurement of Reactive Oxygen Species, Reactive Nitrogen Species, and Redox-Dependent Signaling in the Cardiovascular System: A Scientific Statement From the American Heart Association.Circulation research · 2016Review
- Molecular and Cellular Mechanisms of Cardiovascular Disorders in Diabetes.Circulation research · 2016Review
- Article
- 4-Hydroxy-nonenal-A Bioactive Lipid Peroxidation Product.Biomolecules · 2015Review
- Oxidative and reductive metabolism of lipid-peroxidation derived carbonyls.Chemico-biological interactions · 2015Article
- Aldo-keto Reductase 1B15 (AKR1B15): a mitochondrial human aldo-keto reductase with activity toward steroids and 3-keto-acyl-CoA conjugates.The Journal of biological chemistry · 2015Article
- Lipid peroxidation generates biologically active phospholipids including oxidatively N-modified phospholipids.Chemistry and physics of lipids · 2014Review
- 2013 Russell Ross memorial lecture in vascular biology: cellular and molecular mechanisms of diabetes mellitus-accelerated atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2014Article
- Implications of autophagy for vascular smooth muscle cell function and plasticity.Free radical biology & medicine · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
rationaleAtherosclerotic lesion formation is associated with the accumulation of oxidized lipids. Products of lipid oxidation, particularly aldehydes, stimulate cytokine production and enhance monocyte adhesion; however, their contribution to atherosclerotic lesion formation remains unclear.
objectiveTo test the hypothesis that inhibition of aldehyde removal by aldose reductase (AR), which metabolizes both free and phospholipid aldehydes, exacerbates atherosclerotic lesion formation. METHODS AND
resultsIn atherosclerotic lesions of apolipoprotein (apo)E-null mice, AR protein was located in macrophage-rich regions and its abundance increased with lesion progression. Treatment of apoE-null mice with AR inhibitors sorbinil or tolrestat increased early lesion formation but did not affect the formation of advanced lesions. Early lesions of AR(-/-)/apoE(-/-) mice maintained on high-fat diet were significantly larger when compared with age-matched AR(+/+)/apoE(-/-) mice. The increase in lesion area attributable to deletion of the AR gene was seen in both male and female mice. Pharmacological inhibition or genetic ablation of AR also increased the lesion formation in male mice made diabetic by streptozotocin treatment. Lesions in AR(-/-)/apoE(-/-) mice exhibited increased collagen and macrophage content and a decrease in smooth muscle cells. AR(-/-)/apoE(-/-) mice displayed a greater accumulation of the AR substrate 4-hydroxy trans-2-nonenal (HNE) in the plasma and protein-HNE adducts in arterial lesions than AR(+/+)/apoE(-/-) mice.
conclusionsThese observations indicate that AR is upregulated in atherosclerotic lesions and it protects against early stages of atherogenesis by removing toxic aldehydes generated in oxidized lipids.
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.