Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Int+J+Physiol+Pathophysiol+Pharmacol 2016 ; 8 (1): 28-34 Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Role of autophagy in megakaryocyte differentiation and platelet formation #MMPMID27186320
You T; Wang Q; Zhu L
Int J Physiol Pathophysiol Pharmacol 2016[]; 8 (1): 28-34 PMID27186320show ga
Autophagy is a conserved biological process for digestion and recycling of cytoplasmic constituents in eukaryotic cells. Autophagy may trigger cell death or promote cell survival following various forms of stress. The emerging roles of autophagy in megakaryopoiesis, thrombopoiesis, and platelet function have been uncovered using not only in vitro and in vivo genetic models, but also in clinical observations of autophagic structure in patients with thrombocytopenic disorders. Inhibition of autophagy in early stage of megakaryocyte differentiation appears to impede megakaryocyte maturation, reduce platelet formation, and affect platelet function, whereas autophagic deficiency in mature megakaryocytes gives rise to abnormal platelet activation and function without changing platelet size and number. On the other hand, induction of autophagy by rapamycin in megakaryocytes exhibited substantial therapeutic benefits in patients with immune thrombocytopenic purpura (ITP). This mini-review is to highlight recent progresses in understanding the regulation of autophagy in megakaryopoiesis, thrombopoiesis and platelet function to bridge the gap between autophagy and megakaryocyte/platelet pathophysiology.