Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is concluded on the basis of literature data, that apolipoprotein B-100 is the most high-molecular, hydrophobic, and positive charged protein compared to the other apoproteins of the plasma lipoproteins. Low density lipoproteins of healthy subjects, mainly containing apo B-100, have little heterogeneity on both charge and isoelectric point, in spite of heterogeneity on sizes and apolipoprotein composition. The reason of formation of subfraction with elevated negative charge is the damage with the free radicals and/or aldehydes. The reason of formation of more cationized subfraction is unclear. LDL charge changes are noted in some diseases and syndromes (ischemic heart diseases, familial hyper-alpha-lipoproteinemia, Tangier disease, X-bound ichthyosis and, possibly, others). Some IHD patients treatment with antioxidants leads to the disappearance of negative charged LDL subfraction, that shows participation of peroxidation products in their formation. Electrical characteristics of LDL of tissue fluids and of aorta wall differ essentially from those of the same class plasma lipoproteins. Lipid peroxidation and influences of several enzymes play the main role in these differences.
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PMID:The charge and atherogenicity of low density lipoproteins. 144 71

A low level of high density lipoprotein (HDL) cholesterol is a strong predictor of ischaemic heart disease (IHD) and myocardial infarction. One cause of low HDL-cholesterol is Tangier disease (TD), an autosomal codominant inherited condition first described in 1961 in two siblings on Tangier Island in the United States of America. Apart from low HDL-cholesterol levels and an increased incidence of atherosclerosis, TD is characterized by reduced total cholesterol, raised triglycerides, peripheral neuropathy and accumulation of cholesteryl esters in macrophages, which causes enlargement of the liver, spleen and tonsils. In contrast to two other monogenic HDL deficiencies in which defects in the plasma proteins apoA-I and LCAT interfere primarily with the formation of HDL (refs 7-10), TD shows a defect in cell signalling and the mobilization of cellular lipids. The genetic defect in TD is unknown, and identification of the Tangier gene will contribute to the understanding of this intracellular pathway and of HDL metabolism and its link with IHD. We report here the localization of the genetic defect in TD to chromosome 9q31, using a genome-wide graphical linkage exclusion strategy in one pedigree, complemented by classical lod score calculations at this region in a total of three pedigrees (combined lod 10.05 at D9S1784). We also provide evidence that TD may be due to a loss-of-function defect.
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PMID:Assignment of Tangier disease to chromosome 9q31 by a graphical linkage exclusion strategy. 973 41

Cardiolipin (CL), the signature phospholipid of mitochondrial membranes, is crucial for both mitochondrial function and cellular processes outside of the mitochondria. The importance of CL in cardiovascular health is underscored by the life-threatening genetic disorder Barth syndrome (BTHS), which manifests clinically as cardiomyopathy, skeletal myopathy, neutropenia, and growth retardation. BTHS is caused by mutations in the gene encoding tafazzin, the transacylase that carries out the second CL remodeling step. In addition to BTHS, CL is linked to other cardiovascular diseases (CVDs), including cardiomyopathy, atherosclerosis, myocardial ischemia-reperfusion injury, heart failure, and Tangier disease. The link between CL and CVD may possibly be explained by the physiological roles of CL in pathways that are cardioprotective, including mitochondrial bioenergetics, autophagy/mitophagy, and mitogen activated protein kinase (MAPK) pathways. In this review, we focus on the role of CL in the pathogenesis of CVD as well as the molecular mechanisms that may link CL functions to cardiovascular health.
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PMID:The Role of Cardiolipin in Cardiovascular Health. 2630 Dec 54