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Pathobiochemical Changes of the Arterial Wall at the Inception of Atherosclerosis

  • Chapter
Recent Progress in Atherosclerosis Research

Part of the book series: Current Topics in Pathology ((CT PATHOLOGY,volume 87))

Abstract

The pathogenesis and molecular mechanism of atherosclerosis are still an intriguing and challenging puzzle for cardiovascular research. The potential therapeutic implications of decoding this disease fully justify the efforts to understand the subtle processes which may underlie atherogenesis. Present knowledge does not allow a comprehensive picture of the multiplicity of factors and the sequence of molecular and cellular events which lead to the alterations of the artery wall that generate myocardial and cerebral infarction. Valuable contributions from several laboratories, especially in the last decade, have led to several hypotheses regarding the mechanisms by which elevated serum cholesterol induces atherosclerosis. Among these theories, particularly seminal have been the revised “response-to-injury” (Ross 1986) and the “lipid infiltration” hypotheses, the latter focusing primarily on the role of oxidized low-density lipoprotein (LDL) (Steinberg et al. 1989). Important contributions have also emerged from the laboratories of A. Fogelman, R. Mahley, and others, not to mention the pioneering work on LDL metabolism and LDL receptors, by M. Brown and J. Goldstein. However, focusing the interpretation on a single pathogenic factor can only inadvertently obscure the data accumulate on other lines of investigation and delay the formulation of a coherent theory of atherosclerosis based on generally accepted factual evidence.

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Abbreviations

apo A-I:

apolipoprotein A-I

apo B:

apolipoprotein B

apo E:

apolipoprotein E

ALp:

aggregated lipoproteins

CETP:

cholesteryl ester transfer protein

CSPG:

chondroitin sulfate-proteoglycan

ECs:

endothelial cells

EDRF:

endothelial-derived relaxing factor

ELAM:

endothelial leukocyte adhesion molecules

ELs:

extracellular liposomes

FLp:

fused lipoproteins

FN:

fibronectin

HDL:

high-density lipoproteins

ICAM:

intercellular adhesion molecules

IDL:

intermediate-density lipoproteins

LDL:

low-density lipoproteins

Lp(a):

lipoprotein a

MCP-1:

monocyte chemotactic protein 1

MLp:

monomeric lipoproteins

MM-LDL:

minimally modified LDL

MRLp:

modified and reassembled lipoproteins

OTO:

osmium-thiocarbohydrazideosmium

PAGE:

polyacrylamide gel electrophoresis

TA-PDA:

tannic acid-paraphenylenediamine

VCAM:

vascular cell adhesion molecules

VLDL:

very low-density lipoprotein

VLp:

vesiculated lipoproteitis

WHHL:

Watanabe heritable hyperlipidemic

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  1. N. Simionescu
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  2. A. Sima
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  3. A. Dobrian
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  4. D. Tirziu
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  5. M. Simionescu
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  1. Institut für Pathologie, Otto-von-Guericke-Universität, Leipziger Straße 44, 39120, Magdeburg, Germany

    A. Roessner (Professor Dr.) (Professor Dr.)

  2. Institut für experimentelle Biologie und Medizin, Pathologie, Forschungsinstitut Borstel, Parkalle 40, 23845, Borstel, Germany

    E. Vollmer (Professor Dr. Dr.) (Professor Dr. Dr.)

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Simionescu, N., Sima, A., Dobrian, A., Tirziu, D., Simionescu, M. (1993). Pathobiochemical Changes of the Arterial Wall at the Inception of Atherosclerosis. In: Roessner, A., Vollmer, E. (eds) Recent Progress in Atherosclerosis Research. Current Topics in Pathology, vol 87. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76849-1_1

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