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Pathogenesis of atherosclerosis.
Semin Nephrol. 1996 Jan; 16(1):12-20.SN

Abstract

Atherosclerosis, a common and complex disease, results from multiple interactions among injurious stimuli and the healing or reparative responses of the arterial wall. After endothelial injury, direct cell-cell interaction, and secretion of chemotactic and growth factors resulting from endothelial cell dysfunction, induce recruitment of monocytes to subintimal regions, smooth muscle cell proliferation, and increased synthesis of matrix proteins. The recruited monocytes become macrophages, accumulate lipid, and ultimately become foam cells. Together with accompanying T lymphocytes, these changes represent the fatty streak, an early histopathological change indicating atherosclerosis. Progression of this atherosclerotic lesion is marked by the accumulation of alternating layers of smooth muscle cells and lipid-laden macrophages. The advanced lesions of atherosclerosis compromise the lumen diameter and, thus, reduce the blood flow in arteries and ultimately participate in the mechanisms that lead to occlusion of the involved arteries.

Authors+Show Affiliations

Department of Medicine, University of Minnesota Medical School, Minneapolis, USA.No affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

8720082

Citation

Massy, Z A., and W F. Keane. "Pathogenesis of Atherosclerosis." Seminars in Nephrology, vol. 16, no. 1, 1996, pp. 12-20.
Massy ZA, Keane WF. Pathogenesis of atherosclerosis. Semin Nephrol. 1996;16(1):12-20.
Massy, Z. A., & Keane, W. F. (1996). Pathogenesis of atherosclerosis. Seminars in Nephrology, 16(1), 12-20.
Massy ZA, Keane WF. Pathogenesis of Atherosclerosis. Semin Nephrol. 1996;16(1):12-20. PubMed PMID: 8720082.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Pathogenesis of atherosclerosis. AU - Massy,Z A, AU - Keane,W F, PY - 1996/1/1/pubmed PY - 1996/1/1/medline PY - 1996/1/1/entrez SP - 12 EP - 20 JF - Seminars in nephrology JO - Semin Nephrol VL - 16 IS - 1 N2 - Atherosclerosis, a common and complex disease, results from multiple interactions among injurious stimuli and the healing or reparative responses of the arterial wall. After endothelial injury, direct cell-cell interaction, and secretion of chemotactic and growth factors resulting from endothelial cell dysfunction, induce recruitment of monocytes to subintimal regions, smooth muscle cell proliferation, and increased synthesis of matrix proteins. The recruited monocytes become macrophages, accumulate lipid, and ultimately become foam cells. Together with accompanying T lymphocytes, these changes represent the fatty streak, an early histopathological change indicating atherosclerosis. Progression of this atherosclerotic lesion is marked by the accumulation of alternating layers of smooth muscle cells and lipid-laden macrophages. The advanced lesions of atherosclerosis compromise the lumen diameter and, thus, reduce the blood flow in arteries and ultimately participate in the mechanisms that lead to occlusion of the involved arteries. SN - 0270-9295 UR - https://www.unboundmedicine.com/medline/citation/8720082/Pathogenesis_of_atherosclerosis_ DB - PRIME DP - Unbound Medicine ER -