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Myths of Cholesterol
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2015
Jonny Bowden, Stephen T. Sinatra
Though research starting with the Framingham study has shown a strong positive association between high-plasma HDL and reduced risk of MI, it is not entirely clear if this association is causal. Voight et al.41 used a Mendelian randomization model to test the hypothesis that the association of a plasma biomarker with disease is causal. They found that people who inherit genes (the LIPG 396Ser allele) that naturally give them higher HDL levels have no less heart disease than those who inherit genes that produce slightly lower levels. Though in observational epidemiological studies, a 1 SD increase in HDL cholesterol is associated with reduced risk of MI, the same 1 SD increase due to genetic score was not. The increase in HDL cholesterol associated with the LIPG 396Ser allele would have been expected to produce a 13% decreased risk of MI but in fact was not associated with any reduction in risk. Their data “challenge the concept that raising of plasma HDL cholesterol will uniformly translate into reductions in risk of myocardial infarction.”41
Mechanistic analysis of endothelial lipase G promotion of the occurrence and development of cervical carcinoma by activating the phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B/mechanistic target of rapamycin kinase signalling pathway
Published in Journal of Obstetrics and Gynaecology, 2023
Jing Huang, Renci Liu, Yiwen Zhang, Xiujie Sheng
Lipase G, endothelial type (LIPG) is an important member of the lipase family whose non-enzymatic and enzymatic functions were first reported in 1999 (Jaye et al.1999). LIPG is essential for the malignant features of LIPG-expressing triple negative breast carcinoma (TNBC) cells, including invasiveness, stemness, and basal and epithelial-mesenchyme transition (EMT) features, tumorigenicity, and metastasis in vivo (Lo et al.2018). LIPG is associated with poor prognosis, and high LIPG expression is related to shorter metastasis-free survival (MFS) (Cadenas et al.2019). Studies have shown that LIPG also possesses both enzymatic and non-enzymatic functions in breast cancer cells. The phospholipase function of LIPG is responsible for supporting cell growth and promoting the cell proliferation rate. The phospholipase-independent function of LIPG promotes invasiveness, stemness, and basal/EMT features of breast cancer cells. Although the mechanism by which LIPG executes its non-enzymatic function is unknown, it is likely to act through protein-protein interactions (Lo et al.2020). Treatment with statins to inhibit cholesterol synthesis reduced cisplatin-induced apoptosis, whereas silencing of LIPG or withdrawal of lipids from the culture medium increased sensitivity to the drug (Criscuolo et al.2020). Studies suggest that the synthesis and metabolism of endothelial lipase plays a critical role in tumorigenesis. For example, a recent study stated that elevated LIPG levels are associated with increased risk of breast cancer, especially Luminal A and HER2-negative breast cancers (Gago-Dominguez et al.2021). Considering that a large proportion of the energy comes from fatty acids and that LIPG functions to provide fatty acid precursors, we hypothesised that LIPG plays a role in cervical carcinoma. Consequently, the present study aimed to investigate the mechanism of LIPG in cervical carcinoma.