Role of Stearoyl-CoA Desaturase 1 in Cardiovascular Physiology

Abstract

Stearoyl-CoA desaturase is a rate-limiting enzyme in the synthesis of monounsaturated fatty acids. Monounsaturated fatty acids limit the toxicity of exogenous saturated fats. Studies have shown that stearoyl-CoA desaturase 1 is involved in the remodeling of cardiac metabolism. The loss of stearoyl-CoA desaturase 1 reduces fatty acid oxidation and increases glucose oxidation in the heart. Such a change is protective under conditions of a high-fat diet, which reduces reactive oxygen species-generating β-oxidation. In contrast, stearoyl-CoA desaturase 1 deficiency predisposes individuals to atherosclerosis under conditions of hyperlipidemia but protects against apnea-induced atherosclerosis. Stearoyl-CoA desaturase 1 deficiency also impairs angiogenesis after myocardial infarction. Clinical data show a positive correlation between blood stearoyl-CoA Δ-9 desaturation rates and cardiovascular disease and mortality. Moreover, stearoyl-CoA desaturase inhibition is considered an attractive intervention in some obesity-associated pathologies, and the importance of stearoyl-CoA desaturase in the cardiovascular system might be a limitation for developing such therapy. This review discusses the role of stearoyl-CoA desaturase 1 in the regulation of cardiovascular homeostasis and the development of heart disease and presents markers of systemic stearoyl-CoA desaturase activity and their predictive potential in the diagnosis of cardiovascular disorders.

Development of a novel Guinea Pig model producing transgenerational endothelial transcriptional changes driven by maternal food restriction and a second metabolic insult of high fat diet

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Single-Cell RNA Sequencing Reveals That Adaptation of Human Aortic Endothelial Cells to Antiproliferative Therapies Is Modulated by Flow-Induced Shear Stress

“…Primary pathways negatively enriched by paclitaxel included regulation of EC plasma membrane, such as ankyrin and integrin binding (Figure 3G). Overall, paclitaxel impacts genes related to cell function and vascular integrity (EMCN, by stabilizing the EC barrier and modulating vascular permeability 64 ; SCD, through lipid metabolism 65 ), cell division, cellular intracellular transport, and maintaining cell shape (TUBA1B, TUBB, TUBA1A, and TUBB2A, major members of microtubules of the cytoskeleton 66 ; MAP2, stabilizing microtubules 67 ), apoptosis (ATF4, by modulating amino acid metabolism and antioxidant responses 68 ), and cell proliferation (MALAT1, a long noncoding RNA regulating the expression of other genes 69 ). We substantiated the influence of paclitaxel at the protein level through an analysis of its effects on α-tubulin.…”

Empagliflozin alters lipid metabolism in the myocardium and liver in a prediabetes model with severe dyslipidemia

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