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Dyslipidemia
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
There is a new recommended method of estimating the 10-year and lifetime risk of atherosclerotic CVD. It is based on age, gender, race, total cholesterol and HDL levels, diabetes mellitus, smoking status, and systolic BP. This method is recommended by the American Heart Association. Also, the European Cardiovascular Society and European Atherosclerosis Society use the Systemic Coronary Risk Estimation (SCORE). This method is based on age, gender, smoking, systolic BP, and total cholesterol. It estimates the 10-year risk for a first atherosclerotic event. If a patient is at intermediate risk, lipoprotein(α) should be measured as well. Urinary albuminuria is a strong marker for cardiovascular and noncardiovascular disease and death as well as for renal disorders. Even so, a direct link between albuminuria and atherosclerosis is not fully understood.
Transforming Growth Factor-β: A Cytokine Paradigm
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Michelle R. Frazier-Jessen, Nancy McCartney-Francis, Sharon M. Wahl
Epidemiological studies have demonstrated that elevated levels of Lp(a) are associated with an increased risk for coronary artery disease. Lipoprotein (a) is localized in blood vessel walls and atherosclerotic plaques, both intra- and extracellularly, colocalizing with fibrinogen/fibrin [127]. The underlying mechanism for Lp(a)’s role in atherosclerotic lesions is not completely understood. However, plasminogen shares homology with apoprotein (a) (apo(a)), a glycoprotein component of Lp(a) [128] and, when converted to plasmin, may compete with Lp(a) for binding sites on fibrin. Since plasmin is felt to be the main activator of latent TGF-β in vivo [14], competition between apo(a) and plasminogen could effectively limit the availability of biologically active TGF-β. In transgenic apo(a) mice fed a lipid-rich diet, vascular lesions similar to those observed in early human atherosclerotic plaques develop [129]. While total plasminogen content is not significantly altered in vessel walls of apo(a) mice and normal mice, plasmin content is threefold less in apo(a) mice than in controls. Likewise, while total TGF-β levels are not altered, active TGF-β levels are decreased in both the serum and the vessel wall, where staining for active TGF-β is dramatically diminished at sites of highest apo(a) accumulation within vessel walls.
Physical Activity, Lipids, and Lipoprotein Metabolism: The Benefit of Exercise and Training in Hyperlipidemia
Published in Ronald R. Watson, Marianne Eisinger, Exercise and Disease, 2020
A. Berg, M. Halle, M. Baumstark, I. Frey, J. Keul
The diagnostic criteria of dyslipoproteinemias have been redefined repeatedly during the last few years. They have become independent of merely recognizing elevated serum cholesterol values or lipoprotein fractions of elevated Low Density Lipoproteins (LDL) and reduced levels of High Density Lipoproteins (HDL) in particular. The assessment of the lipoprotein profile has changed since the heterogeneity of atherogenic LDL and cardio-protective HDL particles has been recognized. Among the lipoprotein fraction, LDL and HDL particles have been shown to clearly differ in lipid and apolipoprotein composition, particle size, and physico-chemical properties, and can be influenced differently by endogenous (e.g., genetic) or exogenous (e.g., nutritional, life style) factors (Figure 1).2–5
Human ovarian granulosa cells use clathrin-mediated endocytosis for LDL uptake: immunocytochemical and electron microscopic study
Published in Ultrastructural Pathology, 2023
Aynur Abdulova, Merjem Purelku, Hakan Sahin, Gamze Tanrıverdi
Steroidogenesis is a complex process between multiple enzymes and substrates by which cholesterol is converted into steroid hormones. Cholesterol is stored in lipid droplets (LDs) as cholesterol esters (CEs) within the steroidogenic tissue. The cholesterol that is required for steroidogenesis which is being initiated in response to a hormonal stimulus is provided by the mobilization of these stored CEs within the cells.3 There are two different forms of cholesterol which are known as high-density lipoprotein (HDL) and low-density lipoprotein (LDL). Studies are focused on the fact that granulosa cells use the LDL-receptor (LDLR)-mediated endocytic pathway for steroid biosynthesis. LDLR is an important protein that functions to mediate the uptake of LDL cholesterol, which is a specific substrate for steroid hormone production.3–5 Many different endocytic pathways have been described in eukaryotic cells, but the main pathway for LDL transport has been reported to be the clathrin-mediated endocytosis pathway.6,7 However, no study that clarifies LDL internalization in human granulosa cells and whether the clathrin-mediated endocytic pathway is functional in this process has yet been published.
Focus on cardiometabolic risk factors
Published in Acta Cardiologica, 2023
Assessment of cardiovascular risk using established risk scores such as European Society of Cardiology (ESC) SCORE2 or PROCAM insufficiently emphasise the role of genetic factors. In their study, Krohn et al. showed that both scores failed to adequately discriminate between stable and unstable disease patients with ACS, highlighting the need for optimised risk prediction models involving emerging risk modifiers such as genetic factors or inflammation. Conversely, these authors showed that commercially available assays for genetic polymorphisms may offer useful information on a person’s hereditary risk for CVD, which could help direct future primary and/or secondary preventative therapy for coronary artery disease [14,15]. High plasma concentrations of lipoprotein (a) are associated with an increased cardiovascular risk. Current guidelines recommend the measurement of only a single Lp(a) in an individual’s lifetime under specific circumstances to improve cardiovascular risk prediction. In their study, Deconinck et al. examined the number of false positives and negatives missed through only a single measurement of Lp(a). The authors reported that the determination of Lp(a) was reproducible and that a single measurement was sufficient to assess whether a patient exceeded cut-off values [16] (Figure 2).
Heightened risks of cardiovascular disease in South Asian populations: causes and consequences
Published in Expert Review of Cardiovascular Therapy, 2023
Maria Stefil, Jack Bell, Peter Calvert, Gregory YH Lip
Lipoprotein(a) comprises an LDL particle with apolipoprotein B covalently bound to apolipoprotein(a). Serum lipoprotein(a) levels associate linearly with atherosclerotic ASCVD risk, and as lipoprotein(a) levels are highly genetically determined, they have garnered attention in explaining racial differences in ASCVD risk. Studies to date have had mixed results regarding whether lipoprotein(a) levels are disproportionately elevated in South Asian populations. In the largest study to date, lipoprotein(a) levels from 460,506 individuals registered with the UK biobank were compared between ethnic groups. This study confirmed that lipoprotein(a) levels vary by race with the Black population having the highest median values followed by South Asian, white and Chinese groups (median values 75, 31, 19 and 16 nmol/L, respectively). However, despite this variation in median lipoprotein(a) levels, the risk for atherosclerotic ASCVD per 50 nmol/L increase in lipoprotein(a) appeared similar across ethnic groups[85]. It is important that trials assessing lipoprotein(a)-lowering interventions, such as antisense oligonucleotides, ensure that different ethnic groups are well represented[86].