Lipoproteins are complexes of lipids and proteins that carry water‐insoluble cholesterol in the bloodstream. While cholesterol is required for normal cell function, hypercholesterolemia contributes to the development of cardiovascular disease (CVD). Increased low‐density lipoprotein (LDL) is a major risk factor for CVD. Reduced high‐density lipoprotein (HDL) levels are inversely related to CVD risk, suggesting a protective role for HDL. Several diseases, including atherosclerosis, diabetes, chronic kidney disease and rheumatoid arthritis, have been identified where HDL levels are decreased or function is compromised. HDLs are spherical particles with a hydrophobic core of cholesteryl esters surrounded by a monolayer of phospholipids, proteins and unesterified cholesterol. Apolipoprotein (apo) A‐I, the major protein component of HDL, plays an important role in the assembly and function of HDL. One of the major functions of HDL is to mediate cellular cholesterol efflux and the transfer of cholesterol from extrahepatic tissues to the liver for excretion into the bile. In addition to regulating cholesterol metabolism, HDL also exhibits antioxidative, antithrombotic and anti‐inflammatory properties. Under certain conditions, however, HDL may undergo biochemical modification resulting in the formation of a particle with pro‐inflammatory properties. This review will focus on the variable properties of HDL under normal physiological conditions and in the context of inflammation.
Part of the book: Advances in Lipoprotein Research
Anecdotal and scientific evidence suggest that the sex hormone estrogen provides significant health benefits in women. Women have higher estrogen levels than men. Circulating estrogen reaches its highest level during the reproductive period and steadily declines with the onset of menopause. The role of estrogen and estrogen receptors in both cellular physiology and pathophysiology has been controversial. Estrogen has anti-inflammatory and anti-oxidant effects, which preserve cell viability during cardiovascular incidents, but it enhances disease progression in the context of breast cancer. Estrogen mediates these responses via activation of estrogen receptor subtypes located in the cell membrane, nucleus, and mitochondrion. Further, transcription of nuclear and mitochondrial genes by estrogen yields products that play an important role in regulating mitochondrial function. Mitochondria are part of a highly dynamic network and undergo fission and fusion, produce cellular energy, adenosine 5′ triphosphate (ATP), and regulate cell death. Herein, we review the cell and receptor specific effects of estrogen on mitochondrial structure, function, and cell death under normal physiological conditions and in the context of cardiovascular disease, inflammation, neurodegeneration, and cancer. Further research is needed to elucidate the specific role of estrogenic control of mitochondria in health and disease.
Part of the book: Mitochondrial Diseases