The pathogenesis of atherosclerosis: a perspective for the 1990s

@article{Ross1993ThePO,
  title={The pathogenesis of atherosclerosis: a perspective for the 1990s},
  author={R. Ross},
  journal={Nature},
  year={1993},
  volume={362},
  pages={801-809}
}
  • R. Ross
  • Published 29 April 1993
  • Medicine, Biology
  • Nature
Atherosclerosis, the principal cause of heart attack, stroke and gangrene of the extremities, is responsible for 50% of all mortality in the USA, Europe and Japan. The lesions result from an excessive, inflammatory-fibroproliferative response to various forms of insult to the endothelium and smooth muscle of the artery wall. A large number of growth factors, cytokines and vasoregulatory molecules participate in this process. Our ability to control the expression of genes encoding these… 
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11,137 Citations

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This article attempts to summarize present knowledge on the events that take place within the arterial wall during atherogenesis, with particular emphasis on the cell types involved and the interactions between them.

Development of atherosclerosis and plaque biology.

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Pathobiology of atherosclerosis and plaque complications.

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  • Biology
    American heart journal
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Atherosclerosis: Pathologic Anatomy and Pathogenesis

Atherosclerosis develops as an inflammatory response of the vessel wall to chronic, multifactorial endothelial injury and involves endothelial dysfunction, leukocyte-endothelial cell interactions, intracellular and extracellular accumulation of cholesterol derived from oxidized LDL and smooth musele cell proliferation.

Role of interleukins in atherogenesis

The role interleukins that are released from both immune and non-immune cells of vascular wall may play on the process of atherogenesis are reviewed and it is speculated that these may serve as potential targets for therapeutic intervention.

The role of the endothelium in premature atherosclerosis: Molecular mechanisms.

The inflammation has a key role in the pathophysiological process of the disease and the infiltration of the intima from monocytes, macrophages and T-lymphocytes combined with endothelial dysfunction and accumulated oxidized low-density lipoprotein (LDL) are the main findings of atherogenesis.
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