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Review
. 2011 Feb 1;4(1):104-11.
doi: 10.1161/CIRCINTERVENTIONS.110.957332.

Vascular smooth muscle cell proliferation in restenosis

Steven O Marx  1 , Hana Totary-Jain, Andrew R Marks
Affiliations
Review

Vascular smooth muscle cell proliferation in restenosis

Steven O Marx et al. Circ Cardiovasc Interv. .
No abstract available

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Figures

Figure 1
Figure 1
Schematic of cell cycle. Cell cycle progression is dependent on the regulated expression and activation of a set of kinases (cyclin-dependent kinases, cdk) and cyclins, which phosphorylate proteins that regulate cell growth including the retinoblastoma protein (pRb indicates unphosphorylated; ppRb, phosphorylated form) at the restriction point (R) at the G1/S junction. Cdk inhibitors p27Kip1 and p21Cip1 delay cell cycle progression by inhibiting cdk activity.
Figure 2
Figure 2
Schematic depicting the inhibitory effects of rapamycin and paclitaxel on smooth muscle proliferation.
Figure 3
Figure 3
Combination of PI3K inhibitor (LY294002) and mTOR inhibitor (rapamycin) inhibits leptin-induced neointimal hyperplasia in mice. a, Femoral artery injury. Micrographs of leptin-induced neointimal formation (arrows) in injured femoral arteries after treatment with LY294002 and/or rapamycin. Elastic–van Gieson staining to highlight elastic laminae (black rings) and collagen (red). b, Intima:media (I/M) ratios. Tukey probability values are over brackets. Adapted from Shan J, Nguyen TB, Totary-Jain H, Dansky H, Marx SO, Marks AR. Leptin-enhanced neointimal hyperplasia is reduced by mTOR and PI3K inhibitors. Proc Natl Acad Sci USA. 2008;105:19006 –19011.
See this image and copyright information in PMC

References

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