Lipoproteins and atherosclerosis. A look back and a look ahead.

Steinberg, Daniel

doi:10.1161/01.atv.3.4.283

Cited by 290 publications

(66 citation statements)

References 83 publications

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“…For example, the macrophage interacts extensively with lipoproteins, a topic reviewed by Daniel Steinberg in the 1982 Duff Lecture. 38 Colin Schwartz and his associates recently have identified two other properties of the monocyte-macrophage that may be related to atherogenesis. 39 Monocytes, but not polymorphonuclear leucocytes, are attracted by a substance produced by cultured smooth muscle cells.…”

Section: Monocyte-macrophagementioning

confidence: 99%

George Lyman Duff memorial lecture. Persistent problems in the pathogenesis of atherosclerosis.

McGill¹

1984

Arteriosclerosis

123

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In concluding this eclectic review, I believe that we can say with certainty that coronary atherosclerosis has its origins in childhood, at least by age 10 and possibly earlier. Endothelial changes follow lipid accumulation, but, with present methods, there is no evidence that endothelial injury precedes lipid accumulation. Proliferation is a prominent feature of accelerated experimental atherosclerosis, but we do not see evidence that proliferation is a major feature of early naturally occurring human atherosclerosis. The prominence of the monocyte-macrophage in the earliest detectable lesions of atherosclerosis in childhood justifies the current interest in monocyte biology. Hyperlipidemia, in the sense of the average high levels common in our population, seems almost certain to contribute to accelerated atherogenesis in children, but conclusive proof is still lacking. Mild hypertension in children, or even the high range of normal blood pressure, may accelerate the transition of innocuous childhood fatty streaks to more ominous fibrous plaques. The putative relationship of adult coronary heart disease risk factors to the childhood lesions of atherosclerosis is largely based on extrapolation from adult data. Direct evidence bearing on these relationships, however difficult to obtain, would be helpful in designing and promoting effective preventive regimens for children.

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Section: Monocyte-macrophagementioning

confidence: 99%

George Lyman Duff memorial lecture. Persistent problems in the pathogenesis of atherosclerosis.

McGill¹

1984

Arteriosclerosis

123

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“…Steinberg (1983) argues that elevated plasma concentrations of LDL are alone sufficient to cause atherosclerosis. Patients with homozygous familial hypercholesterolaemia, who have high plasma concentrations of LDL and no other identified risk factors, may suffer from severe atherosclerosis and die from IHD at a very early age.…”

Section: Do Elevated Blood Lipids Cause Atherosclerosis?mentioning

confidence: 99%

Physical Activity, Not Diet, Should be the Focus of Measures for the Primary Prevention of Cardiovascular Disease

Macnair

1994

Nutr. Res. Rev.

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“…It is a complicated process that involves the arterial wall cells, including monocyte-derived macrophages, platelets and plasma lipoproteins. Recent clinical and experimental studies of various kinds have established that elevated plasma concentrations of low-density lipoprotein (LDL) are associated with accelerated atherogenesis (1)(2)(3). Macrophages are especially adopted for cholesterol accumulation derived from cell debris, from platelets, and mainly from plasma lipoproteins, particularly LDL (4).…”

Section: Introductionmentioning

confidence: 99%

Kinetic analysis of LDL oxidation in IHD and IHD risk subjects in Indian population

Gupta

Mallika

Srivastava

2003

Indian J Clin Biochem

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High plasma concentration of low-density lipoprotein (LDL) is associated with increased risk of atherosclerosis. Modified forms of LDL, especially oxidized LDL play a major role in its pathogenesis. This article gives detailed insight into the kinetics of in vitro LDL oxidation by copper at different concentrations in normal and high-risk group subjects. Basal level of oxidatively modified LDL was significantly higher in ischaemic heart disease (IHD) and IHD hyperlipidemic subjects compared to normolipidemic and hyperlipidemic control subjects, respectively. Derivatization of amino groups of apo-lipoprotein as monitored by estimating free amino groups concentration, was significantly higher in high-risk group and established IHD cases. Kinetics of oxidation was studied with two different concentrations of CuSO 4 (2.5 mM and 7.5 mM). Thiobarbituric acid reactive substances (TBARS) level increased with time, and up to 95% oxidation was observed in 8 hr. About 60-65% less free amino groups were observed in native-LDL isolated from IHD patients compared to normal subjects. Study also showed an increase in two oxidative products studied, 20(~-OH-cholesterol and 4-cholesten-3-one with oxidation time accompanied by corresponding decrease in LDL cholesterol. Increase in oxidative species was more evident in high-risk group and IHD patient. Basal level of oxidatively modified LDL measured in terms of TBARS was significantly higher in present study, strongly support that the extent of LDL oxidation monitored as TBARS and FAG level in circulating -LDL could be used as risk marker for high risk group.

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Lipoproteins and atherosclerosis. A look back and a look ahead.

Cited by 290 publications

References 83 publications

George Lyman Duff memorial lecture. Persistent problems in the pathogenesis of atherosclerosis.

George Lyman Duff memorial lecture. Persistent problems in the pathogenesis of atherosclerosis.

Physical Activity, Not Diet, Should be the Focus of Measures for the Primary Prevention of Cardiovascular Disease

Kinetic analysis of LDL oxidation in IHD and IHD risk subjects in Indian population

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