Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The evolution of atheromatous lesions is characterized by its slowness, over on several years, for a long time wholly silent, and by the menace of complications which happened brutally, generally threatening lately the functional and vital prognosis. These complications are: reduction of arterial lumen with its hemodynamic consequences, thromboses, embolisms, and more rarely arterial aneurysms. Atherosclerotic lesions have been known for a long time and well described from the macroscopic and histologic points of view. Likewise, the chemical composition of the arterial components at the different steps of the disease is now known. On the contrary many mysteries still remain concerning the pathogenesis of atherosclerosis, and more and more we tend to think that the causes of the disease are numerous and that they start a number of common mechanisms which begin to be best known.
Sem Hop 1983 Nov 24
PMID:[Atherosclerosis: basic mechanisms]. 632 Mar 86

Disturbances of carbohydrate metabolism due to oral contraceptives appear in diabetics but also in non-diabetics, mainly those who are at high risk for diabetes mellitus (advanced age, obesity, family history, previous abnormality of glucose tolerance). Under oral contraceptives, diabetes mellitus control deteriorates in 30% of all diabetics. Atherosclerosis seems to be accelerated and can lead to serious cardiovascular complications. Reducing the doses of estrogens and progestogens as well as choosing the least diabetogenic progestogen might help to prevent these complications. We believe that micro- or macro-angiopathy is an absolute contraindication of oral contraceptives.
Sem Hop 1983 Dec 08
PMID:[Oral contraceptives, carbohydrate metabolism and diabetes mellitus]. 632 Apr 10

The very rare inherited hypolipoproteinemias are of great help to understand the relations between lipoproteins and atherosclerosis; moreover, in this field, they raise questions, which are discussed in this paper.
Sem Hop 1983 Dec 29
PMID:[Genetic hypolipoproteinemias]. 632 Apr 28

An observation of adrenergic myocarditis with clinical and electrical signs of coronary failure is reported. The patient had electrical and enzymatic manifestations of acute anteroseptal necrosis, complicated at the acute stage by complete atrioventricular block and fatal vasoplegic circulatory collapse. Post-mortem examination showed obstructive atherosclerosis of the anterior interventricular artery without anatomic signs of infarction. Pathogenesis of this coronary failure is discussed. In this case, functional coronary insufficiency produced by catecholamine release was associated with coronary atherosclerosis.
Sem Hop 1984 Mar 29
PMID:[Early coronary atherosclerosis in a malignant pheochromocytoma. Apropos of a case]. 632 81

The molecular mechanisms underlying the relationship between low-density lipoprotein (LDL) and the risk of atherosclerosis are not clear. Therefore, detailed information on the protein composition of LDL may help to reveal its role in atherogenesis. Liquid-phase IEF has been used to resolve LDL proteins into well-defined fractions on the basis of pI, which improves the subsequent detection and resolution of low abundance proteins. Besides known LDL-associated proteins, this approach revealed the presence of proteins not previously described to reside in LDL, including prenylcysteine lyase (PCL1), orosomucoid, retinol-binding protein, and paraoxonase-1. PCL1, an enzyme crucial for the degradation of prenylated proteins, generates free cysteine, isoprenoid aldehyde and hydrogen peroxide. Addition of the substrate farnesylcysteine to lipoprotein resulted in a time-dependent generation of H(2)O(2) which was stronger in very low density lipoprotein (VLDL) than in LDL or HDL, reflecting the greater protein content of PCL1 in VLDL. Farnesol, a dead end inhibitor of the PCL1 reaction, reduced H(2)O(2) generation by VLDL. PCL1 is generated along with nascent lipoprotein, as shown by its presence in the lipoprotein secreted by HepG2 cells. The finding that an enzyme associated with atherogenic lipoproteins can itself generate an oxidant suggests that PCL1 may play a significant role in atherogenesis.
 ...
PMID:Proteomic analysis of human low-density lipoprotein reveals the presence of prenylcysteine lyase, a hydrogen peroxide-generating enzyme. 1925 76

Cardiovascular disorders, like atherosclerosis and hypertension, are increasingly known to be associated with vascular cognitive impairment (VCI). In particular, intracranial atherosclerosis is one of the main causes of VCI, although plaque development occurs later in time and is structurally different compared to atherosclerosis in extracranial arteries. Recent data suggest that endothelial cells (ECs) that line the intracranial arteries may exert anti-atherosclerotic effects due to yet unidentified pathways. To gain insights into underlying mechanisms, we isolated post-mortem endothelial cells from both the intracranial basilar artery (BA) and the extracranial common carotid artery (CCA) from the same individual (total of 15 individuals) with laser capture microdissection. RNA sequencing revealed a distinct molecular signature of the two endothelial cell populations of which the most prominent ones were validated by means of qPCR. Our data reveal for the first time that intracranial artery ECs exert an immune quiescent phenotype. Secondly, genes known to be involved in the response of ECs to damage (inflammation, differentiation, adhesion, proliferation, permeability and oxidative stress) are differentially expressed in intracranial ECs compared to extracranial ECs. Finally, Desmoplakin (DSP) and Hop Homeobox (HOPX), two genes expressed at a higher level in intracranial ECs, and Sodium Voltage-Gated Channel Beta Subunit 3 (SCN3B), a gene expressed at a lower level in intracranial ECs compared to extracranial ECs, were shown to be responsive to shear stress and/or hypoxia. With our data we present a set of intracranial-specific endothelial genes that may contribute to its protective phenotype, thereby supporting proper perfusion and consequently may preserve cognitive function. Deciphering the molecular regulation of the vascular bed in the brain may lead to the identification of novel potential intervention strategies to halt vascular associated disorders, such as atherosclerosis and vascular cognitive dysfunction.
 ...
PMID:Profiling the unique protective properties of intracranial arterial endothelial cells. 3161 Aug 12


<< Previous 1 2