In stent restenosis: bane of the stent era
- Departments of Biomedical Sciences, Medicine, and Medical Microbiology and Immunology, Creighton University School of Medicine, Omaha, NE 68178, NE, USA
- Correspondence to: Professor D K Agrawal Professor of Biomedical Sciences, Medicine, and Medical Microbiology and Immunology, CRISS II Room 510, Creighton University School of Medicine, 2500 California Plaza, Omaha, NE 68178, USA; dkagr{at}creighton.edu
- Accepted 21 June 2005
Abstract
The long term outcome of stent implantation is affected by a process called in stent restenosis (ISR). Multiple contributory factors have been identified, but clear understanding of the overall underlying mechanism remains an enigma. ISR progresses through several different phases and involves numerous cellular and molecular constituents. Platelets and macrophages play a central role via vascular smooth muscle cell migration and proliferation in the intima to produce neointimal hyperplasia, which is pathognomic of ISR. Increased extracellular matrix formation appears to form the bulk of the neointimal hyperplasia tissue. Emerging evidence of the role of inflammatory cytokines and suppressors of cytokine signalling make this an exciting and novel field of antirestenosis research. Activation of Akt pathway triggered by mechanical stretch may also be a contributory factor to ISR formation. Prevention of ISR appears to be a multipronged attack as no therapeutic “magic bullet” exists to block all the processes in one go.
- EC, endothelial cell
- ECM, extracellular matrix
- ER, endoplasmic reticulum
- IAP, inhibitor of apoptosis protein
- IGF, insulin-like growth factor
- ISR, in stent restenosis
- MAPK, mitogen activated protein kinase
- MCP, monocyte chemoattractant protein
- NIH, neo-intimal hyperplasia
- PCNA, proliferating cell nuclear antigen
- PTCA, percutaneous transluminal coronary angioplasty
- SMC, smooth muscle cell
- SOCS, suppressors of cytokine signalling
- TNF, tumour necrosis factor
- TNF-R, TNF receptor
- TUNEL, TdT/dUTP biotin nick end labelling
- VEGF, vascular endothelial growth factor
- VSMC, vascular smooth muscle cell
- apoptosis
- atherosclerosis
- IGF-1
- intimal hyperplasia
- intravascular stenting
- restenosis
- suppressors of cytokine signalling
- vascular smooth muscle cells
