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

Sex hormone deficiency is associated with increased coronary heart disease (CHD) risk in women. We measured fasting serum lipids and lipoprotein concentrations in a group of 542 healthy non-obese pre- and postmenopausal women (aged 18-70 years). Ageing was associated with increased concentrations of total cholesterol, low density lipoprotein (LDL) cholesterol, high density lipoprotein subfraction 3 (HDL3) cholesterol and triglycerides, and decreased concentrations of high density lipoprotein subfraction 2 (HDL2) cholesterol. Body mass index (BMI) was related positively to concentrations of total and LDL cholesterol. Postmenopausal women had significantly higher concentrations of total cholesterol (P < 0.001), triglycerides (P < 0.005), LDL cholesterol (P < 0.001) and high density lipoprotein subfraction 3 (HDL3) cholesterol (P < 0.001), whilst those of HDL and HDL2 cholesterol were significantly lower (P < 0.001). These differences were independent of age, BMI and other potential confounding variables. We conclude that the menopause is associated with potentially adverse changes in lipids and lipoproteins, independent of any effects of ageing. These changes may in part explain the increased incidence of coronary heart disease seen in postmenopausal women.
Atherosclerosis 1993 Jan 04
PMID:Influence of age and menopause on serum lipids and lipoproteins in healthy women. 845 53

Frailty occurs in aging males for a variety of reasons. It is less common in males than females. Diseases which are particularly associated with frailty are diabetes mellitus, atherosclerosis, anemia and chronic obstructive pulmonary disease. Insulin resistance syndrome plays a pathogenetic role in the "fat-frail" syndrome. Sarcopenia occurs predominantly because of hormone deficiency and cytokine excess. Pain and anorexia are also associated with frailty. Stem cell research represents a potential promise for the treatment of frailty.
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PMID:Frailty and the aging male. 1639 Jul 35

Ovarian hormone deficiency increases the generation of reactive oxygen species. Their excess induces oxidative stress, which results in the cell damage or death. It causes the aging diseases-atherosclerosis, rheumatoid arthritis, osteoporosis, etc. Ovariectomized rats are used as oxidative stress models. We verified the effects of ovariectomy-induced oxidative stress on free radical production as evaluated by DPPH elimination, lipoperoxidation evaluated by malondialdehyde levels, and antioxidant activation of superoxide dismutase, catalase, glutathione peroxidase, and estradiol in the liver and sera. Ovariectomized rats were given Salicornia herbacea (SH) intraperitoneally at the dose of 100 mg/kg daily for 2 months. Free radical-scavenging activity of SH was measured in comparison with that of L-ascorbic acid. The histopathology of liver tissue was also investigated. Antioxidative values in the ovariectomized group decreased, but those in the SH-treated group increased due to the free radical-scavenging activity of SH. Moreover, inflammation and cirrhosis in the liver tissue of SH-treated rats decreased significantly. These results suggest that SH may be a potential candidate for an antioxidative reagent.
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PMID:The role of Salicornia herbacea in ovariectomy-induced oxidative stress. 1681 58

The phospholipase neutral sphingomyelinase (N-SMase) has been recognized as a major mediator of processes such as inflammation, development and growth, differentiation and death of cells, as well as in diseases such as Alzheimer's, atherosclerosis, heart failure, ischemia/reperfusion damage, or combined pituitary hormone deficiency. Although activation of N-SMase by the proinflammatory cytokine TNF was described almost two decades ago, the underlying signaling pathway is unresolved. Here, we identify the Polycomb group protein EED (embryonic ectodermal development) as an interaction partner of nSMase2. In yeast, the N terminus of EED binds to the catalytic domain of nSMase2 as well as to RACK1, a protein that modulates the activation of nSMase2 by TNF in concert with the TNF receptor 1 (TNF-R1)-associated protein FAN. In mammalian cells, TNF causes endogenous EED to translocate from the nucleus and to colocalize and physically interact with both endogenous nSMase2 and RACK1. As a consequence, EED and nSMase2 are recruited to the TNF-R1.FAN.RACK1-complex in a timeframe concurrent with activation of nSMase2. After knockdown of EED by RNA interference, the TNF-dependent activation of nSMase2 is completely abrogated, identifying EED as a protein that both physically and functionally couples TNF-R1 to nSMase2, and which therefore represents the "missing link" that completes one of the last unresolved signaling pathways of TNF-R1.
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PMID:The Polycomb group protein EED couples TNF receptor 1 to neutral sphingomyelinase. 2008 May 39

The present study was designed to assess the extent to which vitamin E and aspirin individually or in combination prevent and/or reverse bone loss and atherosclerotic lesion formation in orchidectomized aged rats. Forty-nine 12-month old male Sprague-Dawley rats were either sham-operated (Sham, one group) or orchidectomized (Orx, four groups) and fed a control diet for 120 days to establish bone loss and atherosclerotic lesions. Thereafter, rats were assigned to the various treatment groups (n = 9 to 10 per group): 1) Sham and 2) Orx groups received AIN93M, containing 75 IU vitamin E and served as control, and the other three Orx groups received either 3) 500 IU vitamin E, 4) 500 mg aspirin, or 5) 500 IU vitamin E + 500 mg aspirin per kg diet for 90 days. After 90 days of treatment, rats were sacrificed, necropsied, and tissues were collected for analyses. Results show that 500 IU vitamin E was able to reduce the development of atherosclerosis lesion formation and aortic streak area compared to Orx control. More importantly, 500 mg aspirin completely reversed the fatty streak area and made the atherosclerotic lesions disappear. Vitamin E and aspirin were not able to reverse bone loss as shown by whole body, lumbar and femoral bone mineral content and bone mineral density due to gonadal hormone deficiency. Instead, 500 mg aspirin somewhat increased the trabecular separation while decreased trabecular thickness compared to Orx control. Our findings suggest that both, vitamin E and aspirin exert anti-atherogenic effects and aspirin is more effective than vitamin E in preventing atherosclerosis lesions in Orx rats.
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PMID:Anti-atherogenic properties of vitamin E, aspirin, and their combination. 3035 42