November 29, 2016Journal of Thrombosis and HaemostasisOpen Access

PPARγ agonists negatively regulate αIIbβ3 integrin outside‐in signaling and platelet function through up‐regulation of protein kinase A activity

Q: What is the clinical evidence from this study?

Study design: Other. Intervention: PPARγ agonists. Primary outcome: Platelet adhesion and spreading on fibrinogen and clot retraction.

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Key result

Treatment of platelets with PPARγ agonists inhibited platelet adhesion and spreading on fibrinogen and diminished clot retraction by upregulating protein kinase A activity.

Authors

AUAmanda J. UnsworthUniversity of Leeds NKNeline KriekUniversity of Reading ABAlexander P. ByeUniversity of Reading

Discussion

Member takes

Implication

Does not support clinical antiplatelet use of PPARγ agonists; leaves open mechanistic translation to thrombosis models.

PICO

Intervention / Comparator

PPARγ agonists

Primary Outcome

Platelet adhesion and spreading on fibrinogen and clot retraction

Cite This Study

Unsworth et al. (2016) studied this question. PPARγ agonists was evaluated on Platelet adhesion and spreading on fibrinogen and clot retraction. Treatment of platelets with PPARγ agonists inhibited platelet adhesion and spreading on fibrinogen and diminished clot retraction by upregulating protein kinase A activity.

synapsesocial.com/papers/6a6f2fb35d37378ac1dc4312 https://doi.org/10.1111/jth.13578

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PPARγ agonists negatively regulate αIIbβ3 integrin outside‐in signaling and platelet function through up‐regulation of protein kinase A activity

Discussion

Member takes

Implication

PICO

Cite This Study

PPARγ agonists negatively regulate αIIbβ3 integrin outside‐in signaling and platelet function through up‐regulation of protein kinase A activity

Discussion

Member takes

Implication

PICO

Cite This Study

Also Consider

Also Consider