PMID- 22751382
OWN - NLM
STAT- MEDLINE
DCOM- 20130618
LR  - 20121102
IS  - 1477-111X (Electronic)
IS  - 0267-6591 (Linking)
VI  - 27
IP  - 6
DP  - 2012 Nov
TI  - Intimal hyperplasia: slow but deadly.
PG  - 520-8
LID - 10.1177/0267659112452316 [doi]
AB  - Intimal hyperplasia is the leading cause of long-term failure in coronary artery 
      bypass vein grafting, coronary artery stenting, angioplasty, arteriovenous 
      fistula for dialysis, and allograft transplantation. Intimal hyperplasia is a 
      product of vascular smooth muscle cell proliferation, migration through the 
      internal elastic lamina, and deposition of extracellular matrix proteins driven 
      by growth factors in the vasculature. This vascular pathology results in a 
      progressive diminution of the vessel lumen and serves as a site for thrombosis 
      and atherosclerotic lesions. A key cell type in the initiation of intimal 
      hyperplasia is the vascular endothelial cell, which appears to have down-stream 
      effects on the vascular smooth muscle proliferation and migration. Currently, the 
      only means available for prevention of intimal hyperplasia is through inhibition 
      of mammalian target of rapamycin (mTOR) with the immunosuppressant rapamycin. 
      mTOR integrates up-stream signals from growth factors such as IL-2 and senses the 
      cellular nutrient and energy levels and redox status. This presentation will 
      discuss the potential means of preserving the vascular endothelial cell and, 
      thereby, reducing the development of intimal hyperplasia in our open-heart 
      surgical patients.
FAU - Mills, B
AU  - Mills B
AD  - Circulatory Sciences Graduate Perfusion Program, The University of Arizona, 
      Tucson, AZ, USA.
FAU - Robb, T
AU  - Robb T
FAU - Larson, D F
AU  - Larson DF
LA  - eng
GR  - R01HL105280-02/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20120629
PL  - England
TA  - Perfusion
JT  - Perfusion
JID - 8700166
SB  - IM
CIN - Perfusion. 2012 Nov;27(6):529. PMID: 23118127
MH  - Cell Growth Processes/drug effects/physiology
MH  - Humans
MH  - Hyperplasia
MH  - Muscle, Smooth, Vascular/drug effects/pathology
MH  - Tunica Intima/drug effects/*pathology
MH  - Vascular Diseases/*pathology/therapy
EDAT- 2012/07/04 06:00
MHDA- 2013/06/19 06:00
CRDT- 2012/07/04 06:00
PHST- 2012/07/04 06:00 [entrez]
PHST- 2012/07/04 06:00 [pubmed]
PHST- 2013/06/19 06:00 [medline]
AID - 0267659112452316 [pii]
AID - 10.1177/0267659112452316 [doi]
PST - ppublish
SO  - Perfusion. 2012 Nov;27(6):520-8. doi: 10.1177/0267659112452316. Epub 2012 Jun 29.