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Renal Klotho safeguards platelet lifespan in advanced chronic kidney disease through restraining Bcl‐xL ubiquitination and degradation

Renal Klotho safeguards platelet lifespan in advanced chronic kidney disease through restraining... EssentialsThe mechanisms underlying platelet disorders in chronic kidney disease (CKD) are poorly understood.We examined platelet homeostasis in CKD and its association with renal Klotho deficiency.p38MAPK/UBE2O–mediated Bcl‐xL ubiquitination and degradation shorten platelet lifespan in CKD.Renal Klotho safeguards platelet lifespan through restraining the p38MAPK/UBE2O axis.INTRODUCTIONChronic kidney disease (CKD) is a global public health issue with increasing mortality and morbidity. It has been well recognized that thrombotic disease is a prevalent complication of CKD.1 Surprisingly, CKD is also associated with an enhanced risk of hemorrhage, and the risk of major hemorrhage increases in a graded fashion with renal function decline.2 Moreover, advanced CKD (Adv‐CKD) patients, especially those who initiate chronic dialysis, are even suffering from a much higher incidence of hemorrhagic events.2,3 Unfortunately, it remains hard, to date, to understand why these two opposite pathologies co‐exist within the CKD population. Meanwhile, there is a substantial unmet clinical need for effective measures to predict and manage these two opposite but equally fatal complications.Thrombosis and hemostasis are principally determined by the number and function of circulating platelets.4 Currently, reports on platelet function in relation to CKD are conflicting, varying from decreased to normal or even enhanced platelet reactivity, making the co‐existence of thrombotic and http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Thrombosis and Haemostasis Wiley

Renal Klotho safeguards platelet lifespan in advanced chronic kidney disease through restraining Bcl‐xL ubiquitination and degradation

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References (49)

Publisher
Wiley
Copyright
© 2022 International Society on Thrombosis and Haemostasis
ISSN
1538-7933
eISSN
1538-7836
DOI
10.1111/jth.15876
Publisher site
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Abstract

EssentialsThe mechanisms underlying platelet disorders in chronic kidney disease (CKD) are poorly understood.We examined platelet homeostasis in CKD and its association with renal Klotho deficiency.p38MAPK/UBE2O–mediated Bcl‐xL ubiquitination and degradation shorten platelet lifespan in CKD.Renal Klotho safeguards platelet lifespan through restraining the p38MAPK/UBE2O axis.INTRODUCTIONChronic kidney disease (CKD) is a global public health issue with increasing mortality and morbidity. It has been well recognized that thrombotic disease is a prevalent complication of CKD.1 Surprisingly, CKD is also associated with an enhanced risk of hemorrhage, and the risk of major hemorrhage increases in a graded fashion with renal function decline.2 Moreover, advanced CKD (Adv‐CKD) patients, especially those who initiate chronic dialysis, are even suffering from a much higher incidence of hemorrhagic events.2,3 Unfortunately, it remains hard, to date, to understand why these two opposite pathologies co‐exist within the CKD population. Meanwhile, there is a substantial unmet clinical need for effective measures to predict and manage these two opposite but equally fatal complications.Thrombosis and hemostasis are principally determined by the number and function of circulating platelets.4 Currently, reports on platelet function in relation to CKD are conflicting, varying from decreased to normal or even enhanced platelet reactivity, making the co‐existence of thrombotic and

Journal

Journal of Thrombosis and Haemostasis – Wiley

Published: Dec 1, 2022

Keywords: Bcl‐xL; chronic kidney disease; Klotho; platelets; UBE2O

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