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Review

Reflections on Atherosclerosis: Lesson from the Past and Future Research Directions

ORCID Icon, ORCID Icon & ORCID Icon
Pages 621-633 | Published online: 17 Jul 2020

Figures & data

Figure 1 Rudolf Virchow (1821–1902).

Note: Photo courtesy of Carl Günther (public domain).Citation105

Figure 1 Rudolf Virchow (1821–1902).Note: Photo courtesy of Carl Günther (public domain).Citation105

Figure 2 Carl von Rokitansky (1804–1878).

Note: Photo courtesy of Adolf Dauthage (public domain).Citation106

Figure 2 Carl von Rokitansky (1804–1878).Note: Photo courtesy of Adolf Dauthage (public domain).Citation106

Figure 3 Schematic of atherogenesis.

Notes: The oxidized-LDLs induce the activation of endothelial cells and the expression of various leukocyte adhesion molecules (such as VCAM1) and consequent monocyte adhesion to the endothelium (1,2); subsequent transmigration of monocytes into the intima, where they differentiate into macrophages (3,4); T lymphocytes join macrophages in the intima during plaque evolution (5); macrophages, incorporating modified lipoproteins, become lipid-rich foam cells (6); the inflammatory response stimulates migration and replication of vascular smooth muscle cells, which accumulate in the plaque to form a fibroproliferative lesion (7,8); macrophages in the plaque show abnormal lipid metabolism with a reduction of the cholesterol efflux, (9) which leads to accumulation of apoptotic bodies and necrotic debris, forming a necrotic core (10). ©[designua]/123RF.COM

Figure 3 Schematic of atherogenesis.Notes: The oxidized-LDLs induce the activation of endothelial cells and the expression of various leukocyte adhesion molecules (such as VCAM1) and consequent monocyte adhesion to the endothelium (1,2); subsequent transmigration of monocytes into the intima, where they differentiate into macrophages (3,4); T lymphocytes join macrophages in the intima during plaque evolution (5); macrophages, incorporating modified lipoproteins, become lipid-rich foam cells (6); the inflammatory response stimulates migration and replication of vascular smooth muscle cells, which accumulate in the plaque to form a fibroproliferative lesion (7,8); macrophages in the plaque show abnormal lipid metabolism with a reduction of the cholesterol efflux, (9) which leads to accumulation of apoptotic bodies and necrotic debris, forming a necrotic core (10). ©[designua]/123RF.COM