The timing of onset of pathological thrombotic events, including myocardial infarction and stroke, display a cyclic pattern with peak incidence between 6am and noon. Such a 24 hr pattern suggests that a circadian “timer” contributes to thrombosis. However, a gap still exists in understanding the molecular mechanisms linking timing systems to disease events. A major hypothesis of this proposal is that the internal circadian clock plays a key role in hemostasis, and that disruption of circadian systems contributes to thrombotic events.
|Effective start/end date||1/1/13 → 12/31/13|
- Endocrine Fellows Foundation (Award Letter 10/31/12)
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