PMID- 37511848
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230801
IS  - 2075-1729 (Print)
IS  - 2075-1729 (Electronic)
IS  - 2075-1729 (Linking)
VI  - 13
IP  - 7
DP  - 2023 Jun 29
TI  - Platelet Glycoprotein-Ib (GPIb) May Serve as a Bridge between Type 2 Diabetes 
      Mellitus (T2DM) and Atherosclerosis, Making It a Potential Target for 
      Antiplatelet Agents in T2DM Patients.
LID - 10.3390/life13071473 [doi]
LID - 1473
AB  - Type 2 diabetes mellitus (T2DM) is a persistent metabolic condition that 
      contributes to the development of cardiovascular diseases. Numerous studies have 
      provided evidence that individuals with T2DM are at a greater risk of developing 
      cardiovascular diseases, typically two to four times more likely than those 
      without T2DM, mainly due to an increased risk of atherosclerosis. The rupture of 
      an atherosclerotic plaque leading to pathological thrombosis is commonly 
      recognized as a significant factor in advancing cardiovascular diseases caused by 
      TD2M, with platelets inducing the impact of plaque rupture in established 
      atherosclerosis and predisposing to the primary expansion of atherosclerosis. 
      Studies suggest that individuals with T2DM have platelets that display higher 
      baseline activation and reactivity than those without the condition. The 
      expression enhancement of several platelet receptors is known to regulate 
      platelet activation signaling, including platelet glycoprotein-Ib (GPIb). 
      Furthermore, the high expression of platelet GP1b has been reported to increase 
      the risk of platelet adhesion, platelet-leucocyte interaction, and 
      thrombo-inflammatory pathology. However, the study exploring the role of GP1b in 
      promoting platelet activation-induced cardiovascular diseases in T2DM patients is 
      still limited. Therefore, we summarize the important findings regarding 
      pathophysiological continuity between T2DM, platelet GPIb, and atherosclerosis 
      and highlight the potential therapy targeting GPIb as a novel antiplatelet agent 
      for preventing further cardiovascular incidents in TD2M patients.
FAU - Amalia, Muttia
AU  - Amalia M
AD  - Doctoral Program, Faculty of Pharmacy, Universitas Indonesia, Kampus UI Depok, 
      Depok 16424, Indonesia.
FAU - Puteri, Meidi Utami
AU  - Puteri MU
AUID- ORCID: 0000-0003-1550-8627
AD  - Laboratory of Pharmacology-Toxicology, Faculty of Pharmacy, Universitas 
      Indonesia, Kampus UI Depok, Depok 16424, Indonesia.
FAU - Saputri, Fadlina Chany
AU  - Saputri FC
AUID- ORCID: 0000-0002-6668-8915
AD  - Laboratory of Pharmacology-Toxicology, Faculty of Pharmacy, Universitas 
      Indonesia, Kampus UI Depok, Depok 16424, Indonesia.
FAU - Sauriasari, Rani
AU  - Sauriasari R
AD  - Faculty of Pharmacy, Universitas Indonesia, Kampus UI Depok, Depok 16424, 
      Indonesia.
FAU - Widyantoro, Bambang
AU  - Widyantoro B
AD  - National Cardiovascular Center Harapan Kita, Department of Cardiology and 
      Vascular Medicine, Faculty of Medicine, Universitas Indonesia, Jakarta 11420, 
      Indonesia.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20230629
PL  - Switzerland
TA  - Life (Basel)
JT  - Life (Basel, Switzerland)
JID - 101580444
PMC - PMC10381765
OTO - NOTNLM
OT  - antiplatelet
OT  - atherosclerosis
OT  - glycoprotein-Ib (GP1b)
OT  - platelet
OT  - type 2 diabetes mellitus (T2DM)
COIS- The authors declare no conflict of interest.
EDAT- 2023/07/29 11:47
MHDA- 2023/07/29 11:48
PMCR- 2023/06/29
CRDT- 2023/07/29 01:26
PHST- 2023/05/29 00:00 [received]
PHST- 2023/06/23 00:00 [revised]
PHST- 2023/06/26 00:00 [accepted]
PHST- 2023/07/29 11:48 [medline]
PHST- 2023/07/29 11:47 [pubmed]
PHST- 2023/07/29 01:26 [entrez]
PHST- 2023/06/29 00:00 [pmc-release]
AID - life13071473 [pii]
AID - life-13-01473 [pii]
AID - 10.3390/life13071473 [doi]
PST - epublish
SO  - Life (Basel). 2023 Jun 29;13(7):1473. doi: 10.3390/life13071473.