Pathobiology of intimal hyperplasia

Davies, Mark G.; Hagen, Per Otto

doi:10.1002/bjs.1800810904

Cited by 400 publications

(301 citation statements)

References 187 publications

Supporting

Mentioning

276

Contrasting

Unclassified

Order By: Relevance

“…4 The intimal thickening that occurs after placing the vein into the arterial circulation, is due to the accumulation of smooth muscle cells (SMCs) and deposition of extracellular matrix in the intima. 5 Accumulation of SMCs in the intima is due to the migration of SMCs from the media to the intima where they subsequently proliferate.…”

Section: Introductionmentioning

confidence: 99%

Wild-type p53 gene transfer inhibits neointima formation in human saphenous vein by modulation of smooth muscle cell migration and induction of apoptosis

et al. 2001

View full text Add to dashboard Cite

Patency of autologous human saphenous vein coronary artery bypass grafts (CABG) is compromised by intimal thickening and superimposed atherosclerosis, caused by migration of vascular smooth muscle cells (SMC) to the intima where they proliferate. Here, using adenoviral transfer, we have targeted SMCs using wild-type p53 (wt p53) overexpression. Initial in vitro analyses demonstrated that wt p53 overexpression had no effect on SMC proliferation but promoted apoptosis, which was inhibited by co-expression of bcl2 or crmA. Wt p53 inhibited SMC invasion through reconstituted matrices, a phenotype not affected by bcl2 or crmA. Overexpression of wt p53 in human saphenous vein

show abstract

Section: Introductionmentioning

confidence: 99%

Wild-type p53 gene transfer inhibits neointima formation in human saphenous vein by modulation of smooth muscle cell migration and induction of apoptosis

et al. 2001

View full text Add to dashboard Cite

show abstract

“…Lumenal narrowing and superimposition of atheroma on the thickened intima promote thrombotic occlusion and hence account for the poor patency rates observed. [3][4][5] The matrix metalloproteinases (MMPs) have the ability to degrade all components of the basement membrane and the interstitial matrix. 6 Increased proteolysis by MMPs has been associated with cancer cell invasion, rheumatoid arthritis and more recently with the neointima formation that characterises vascular diseases.…”

Section: Introductionmentioning

confidence: 99%

Gene transfer of tissue inhibitor of metalloproteinase-2 inhibits metalloproteinase activity and neointima formation in human saphenous veins

et al. 1998

View full text Add to dashboard Cite

Metalloproteinases (MMPs) are implicated in neointima for-21.8 ± 2.9 ng/mg wet weight/day (P Ͻ 0.05, n = 3). In situ mation and hence vein graft failure. Gene transfer to elevzymography revealed a marked inhibition of gelatinolytic ate local levels of tissue inhibitor of metalloproteinases activity by TIMP-2 gene transfer throughout the vein seg-(TIMPs) is therefore a potential treatment. In this study, we ments. Neointima formation and neointimal cell numbers have used lumenal application of a replication-defective were reduced 79% and 71%, respectively (P Ͻ 0.05; recombinant adenovirus to overexpress TIMP-2 and n = 8). TIMP-2 overexpression had no effect on smooth observe the effects on neointimal thickening in a well muscle cell proliferation, secretion of pro-MMP-2 or -9 and characterised human saphenous vein organ culture model.did not inhibit the processing of pro-MMP-2 to its active Increased TIMP-2 expression was localised to lumenal form. Our data indicate that TIMP-2 overexpression surface cells but nevertheless increased total functional reduces neointimal thickening, primarily by inhibiting MMP TIMP-2 secretion after 14 days culture from 4.0 ± 2.0 to activity and hence smooth muscle cell migration.

show abstract

“…The pathogenic mechanisms of atheroma remain elusive and few effective techniques are available to prevent this event. [1][2][3] Hypercholesterolemia has been shown to be a significant risk factor for the development of vein graft atheroma. 4 Evidence indicates that rates of obstructive atheroma in grafted veins were highly correlated to preoperative serum cholesterol levels, 5 and that the lesion development was predicted by higher levels of plasma very low density lipoprotein (VLDL) and low density lipoprotein (LDL).…”

mentioning

confidence: 99%