PMID- 23634936
OWN - NLM
STAT- MEDLINE
DCOM- 20130619
LR  - 20130502
IS  - 1470-8736 (Electronic)
IS  - 0143-5221 (Linking)
VI  - 125
IP  - 4
DP  - 2013 Aug
TI  - The vascular smooth muscle cell: a therapeutic target in Type 2 diabetes?
PG  - 167-82
LID - 10.1042/CS20120413 [doi]
AB  - The rising epidemic of T2DM (Type 2 diabetes mellitus) worldwide is of 
      significant concern. The inherently silent nature of the disease in its early 
      stages precludes early detection; hence cardiovascular disease is often 
      established by the time diabetes is diagnosed. This increased cardiovascular risk 
      leads to significant morbidity and mortality in these individuals. Progressive 
      development of complications as a result of previous exposure to metabolic 
      disturbances appears to leave a long-lasting impression on cells of the 
      vasculature that is not easily reversed and is termed 'metabolic memory'. SMCs 
      (smooth muscle cells) of blood vessel walls, through their inherent ability to 
      switch between a contractile quiescent phenotype and an active secretory state, 
      maintain vascular homoeostasis in health and development. This plasticity also 
      confers SMCs with the essential capacity to adapt and remodel in pathological 
      states. Emerging clinical and experimental studies propose that SMCs in diabetes 
      may be functionally impaired and thus contribute to the increased incidence of 
      macrovascular complications. Although this idea has general support, the 
      underlying molecular mechanisms are currently unknown and hence are the subject 
      of intense research. The aim of the present review is to explore and evaluate the 
      current literature relating to the problem of vascular disease in T2DM and to 
      discuss the critical role of SMCs in vascular remodelling. Possibilities for 
      therapeutic strategies specifically at the level of T2DM SMCs, including recent 
      novel advances in the areas of microRNAs and epigenetics, will be evaluated. 
      Since restoring glucose control in diabetic patients has limited effect in 
      ameliorating their cardiovascular risk, discovering alternative strategies that 
      restrict or reverse disease progression is vital. Current research in this area 
      will be discussed.
FAU - Porter, Karen E
AU  - Porter KE
AD  - Division of Cardiovascular & Diabetes Research, Leeds Institute of Genetics, 
      Health and Therapeutics (LIGHT), University of Leeds, Leeds LS2 9JT, UK. 
      k.e.porter@leeds.ac.uk
FAU - Riches, Kirsten
AU  - Riches K
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Clin Sci (Lond)
JT  - Clinical science (London, England : 1979)
JID - 7905731
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (MicroRNAs)
SB  - IM
MH  - Animals
MH  - Cardiovascular Diseases/etiology/*pathology/therapy
MH  - Diabetes Mellitus, Experimental/complications/pathology
MH  - Diabetes Mellitus, Type 2/complications/*pathology/therapy
MH  - Endothelium, Vascular/pathology/physiopathology
MH  - Epigenesis, Genetic
MH  - Humans
MH  - Hypoglycemic Agents/therapeutic use
MH  - MicroRNAs/genetics/metabolism
MH  - Molecular Targeted Therapy
MH  - Muscle, Smooth, Vascular/*pathology/physiopathology
MH  - Myocytes, Smooth Muscle/*pathology/physiology
MH  - Risk
EDAT- 2013/05/03 06:00
MHDA- 2013/06/20 06:00
CRDT- 2013/05/03 06:00
PHST- 2013/05/03 06:00 [entrez]
PHST- 2013/05/03 06:00 [pubmed]
PHST- 2013/06/20 06:00 [medline]
AID - CS20120413 [pii]
AID - 10.1042/CS20120413 [doi]
PST - ppublish
SO  - Clin Sci (Lond). 2013 Aug;125(4):167-82. doi: 10.1042/CS20120413.