ArticleAtherosclerosis2010
Genetic reduction of lipoic acid synthase expression modestly increases atherosclerosis in male, but not in female, apolipoprotein E-deficient mice.
Article in Atherosclerosis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Cystine: A Key Protective Factor Against Childhood Hypo-HDL Cholesterolemia and Dyslipidemia-A Matched Case-Control Study.Nutrients · 2026Observational
- Deciphering the Role of Copper Homeostasis in Atherosclerosis: From Molecular Mechanisms to Therapeutic Targets.International journal of molecular sciences · 2024Review
- Construction and validation of a cuproptosis-related diagnostic gene signature for atrial fibrillation based on ensemble learning.Hereditas · 2023Article
- Cuproptosis-a potential target for the treatment of osteoporosis.Frontiers in endocrinology · 2023Review
- Overexpression of lipoic acid synthase gene alleviates diabetic nephropathyBMJ open diabetes research & care · 2021Article
- Diet alters age-related remodeling of aortic collagen in mice susceptible to atherosclerosis.American journal of physiology. Heart and circulatory physiology · 2021Article
- Disparate Modes of Evolution Shaped Modern Prion (PRNP) and Prion-Related Doppel (PRND) Variation in Domestic Cattle.PloS one · 2016Article
- α-Lipoic acid protects mitochondrial enzymes and attenuates lipopolysaccharide-induced hypothermia in mice.Free radical biology & medicine · 2014Article
- Reduced alpha-lipoic acid synthase gene expression exacerbates atherosclerosis in diabetic apolipoprotein E-deficient mice.Atherosclerosis · 2012Article
- α-Lipoic acid protects diabetic apolipoprotein E-deficient mice from nephropathy.Journal of diabetes and its complicationsArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectivesTo evaluate the effects of a genetic reduction of Lias gene expression on atherosclerosis development. METHODS AND
resultsHeterozygous knockout mice for the lipoid acid synthase gene (Lias(+/-)) were crossed with apolipoprotein E-deficient (ApoE(-/-)) mice, and the plaque size in aortic sinuses of Lias(+/-)ApoE(-/-)mice was evaluated at 6 months of age. Lesions at the aortic sinus in Lias(+/-)ApoE(-/-) males were significantly larger (1.5x) than those in Lias(+/+) ApoE(-/-) littermate males. The lesion size was inversely correlated with an increased erythrocyte reduced glutathione/oxidized glutathione (GSH/GSSH) ratio, a systemic index of body redox balance. Lias(+/-)ApoE(-/-)males also had significantly increased plasma cholesterol and reduced pyruvate dehydrogenase complex activity in the liver. Significant reductions in the expression of genes for antioxidant enzymes, including superoxide dismutase 1 (SOD1) and SOD2, were observed in aortas of Lias(+/-)ApoE(-/-)males. Female Lias(+/-)ApoE(-/-)also exhibited changes in these parameters, parallel to those observed in males. However, the Lias gene effects for the majority of these factors, including atherosclerotic lesion size, were not significant in females.
conclusionsOur data provide evidence that Lias deficiency enhances atherosclerosis in male mice, at least in part due to reduced antioxidant capacity. The notable absence of such effects in females leaves open the possibility of a gender-specific protection mechanism.
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