PMID- 25601838
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20150120
LR  - 20220408
IS  - 1664-042X (Print)
IS  - 1664-042X (Electronic)
IS  - 1664-042X (Linking)
VI  - 5
DP  - 2014
TI  - Platelet hemostasis in patients with metabolic syndrome and type 2 diabetes 
      mellitus: cGMP- and NO-dependent mechanisms in the insulin-mediated platelet 
      aggregation.
PG  - 501
LID - 10.3389/fphys.2014.00501 [doi]
LID - 501
AB  - Patients with metabolic syndrome (MetS) and type 2 diabetes mellitus (T2DM) have 
      high risk of microcirculation complications and microangiopathies. An increase in 
      thrombogenic risk is associated with platelet hyperaggregation, hypercoagulation, 
      and hyperfibrinolysis. Factors leading to platelet activation in MetS and T2DM 
      comprise insulin resistance, hyperglycemia, non-enzymatic glycosylation, 
      oxidative stress, and inflammation. This review discusses the role of nitric 
      oxide (NO) in the regulation of platelet adhesion and aggregation processes. NO 
      is synthesized both in endotheliocytes, smooth muscle cells, macrophages, and 
      platelets. Modification of platelet NO-synthase (NOS) activity in MetS patients 
      can play a central role in the manifestation of platelet hyperactivation. 
      Metabolic changes, accompanying T2DM, can lead to an abnormal NOS expression and 
      activity in platelets. Hyperhomocysteinemia, often accompanying T2DM, is a risk 
      factor for cardiovascular accidents. Homocysteine can reduce NO production by 
      platelets. This review provides data on the insulin effects in platelets. 
      Decrease in a number and sensitivity of the insulin receptors on platelets in 
      T2DM can cause platelet hyperactivation. Various intracellular mechanisms of 
      anti-aggregating insulin effects are discussed. Anti-aggregating effects of 
      insulin are mediated by a NO-induced elevation of cGMP and upregulation of cAMP- 
      and cGMP-dependent pathways. The review presents data suggesting an ability of 
      platelets to synthesize humoral factors stimulating thrombogenesis and 
      inflammation. Proinflammatory cytokines are considered as markers of T2DM and 
      cardiovascular complications and are involved in the development of dyslipidemia 
      and insulin resistance. The article provides an evaluation of NO-mediated 
      signaling pathway in the effects of cytokines on platelet aggregation. The 
      effects of the proinflammatory cytokines on functional activity of platelets are 
      demonstrated.
FAU - Suslova, Tatiana E
AU  - Suslova TE
AD  - Federal State Budgetary Scientific Institution "Research Institute for 
      Cardiology," Tomsk, Russia ; Center of High Technology in the Medicine, 
      Laboratory for Translational Cellular and Molecular Biomedicine, National 
      Research Tomsk State University Tomsk, Russia.
FAU - Sitozhevskii, Alexei V
AU  - Sitozhevskii AV
AD  - Federal State Budgetary Scientific Institution "Research Institute for 
      Cardiology," Tomsk, Russia.
FAU - Ogurkova, Oksana N
AU  - Ogurkova ON
AD  - Federal State Budgetary Scientific Institution "Research Institute for 
      Cardiology," Tomsk, Russia.
FAU - Kravchenko, Elena S
AU  - Kravchenko ES
AD  - Federal State Budgetary Scientific Institution "Research Institute for 
      Cardiology," Tomsk, Russia.
FAU - Kologrivova, Irina V
AU  - Kologrivova IV
AD  - Federal State Budgetary Scientific Institution "Research Institute for 
      Cardiology," Tomsk, Russia.
FAU - Anfinogenova, Yana
AU  - Anfinogenova Y
AD  - Federal State Budgetary Scientific Institution "Research Institute for 
      Cardiology," Tomsk, Russia ; Institute of Physics and Technology, National 
      Research Tomsk Polytechnic University Tomsk, Russia.
FAU - Karpov, Rostislav S
AU  - Karpov RS
AD  - Federal State Budgetary Scientific Institution "Research Institute for 
      Cardiology," Tomsk, Russia.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20150105
PL  - Switzerland
TA  - Front Physiol
JT  - Frontiers in physiology
JID - 101549006
PMC - PMC4283519
OTO - NOTNLM
OT  - cyclic guanosine monophosphate
OT  - metabolic syndrome
OT  - nitric oxide
OT  - nitric oxide synthase
OT  - platelets
OT  - type 2 diabetes mellitus
EDAT- 2015/01/21 06:00
MHDA- 2015/01/21 06:01
PMCR- 2015/01/05
CRDT- 2015/01/21 06:00
PHST- 2014/09/10 00:00 [received]
PHST- 2014/12/02 00:00 [accepted]
PHST- 2015/01/21 06:00 [entrez]
PHST- 2015/01/21 06:00 [pubmed]
PHST- 2015/01/21 06:01 [medline]
PHST- 2015/01/05 00:00 [pmc-release]
AID - 10.3389/fphys.2014.00501 [doi]
PST - epublish
SO  - Front Physiol. 2015 Jan 5;5:501. doi: 10.3389/fphys.2014.00501. eCollection 2014.