A thromboprotective mechanism common to hibernating bears and chronically paralyzed humans provides a target for development of VTE prevention therapies.
Immobility is known to predispose people to venous thromboembolism (VTE). It is a key component of Virchow's triad and has been taught as a classic risk factor for VTE. So, why is it that hibernating bears, being immobile for months, do not manifest an excess risk of venous thrombosis? At first glance, this question may seem irrelevant for clinicians, but a new investigation into the answer makes an elegant link with clinical care.
In this multicomponent translational study, the authors performed a proteomics analysis of venous blood from hibernating brown bears, comparing results with summertime blood samples. They discovered that heat shock protein 47 (HSP47) was substantially downregulated (55-fold) in platelets of hibernating bears (at l…
Reviewing Author
DisclosuresGrant/Research SupportBrigham and Women’s Hospital; American Heart Association and VIVA Physicians
Editorial BoardsThrombosis Research; Thrombosis and Haemostasis; Journal of the American College of Cardiology
Leadership Positions in Professional SocietiesSociety for Vascular Medicine (Research, Quality, and Publications Committee member); International Society on Thrombosis and Haemostasis
DisclosuresGrant/Research SupportBrigham and Women’s Hospital; American Heart Association and VIVA Physicians
Editorial BoardsThrombosis Research; Thrombosis and Haemostasis; Journal of the American College of Cardiology
Leadership Positions in Professional SocietiesSociety for Vascular Medicine (Research, Quality, and Publications Committee member); International Society on Thrombosis and Haemostasis