Autophagy as a Regulatory Component of Erythropoiesis

International Journal of Molecular Sciences

Jieying Zhang³  Kunlu Wu³  Xiaojuan Xiao³  Jiling Liao³  Qikang Hu³  Huiyong Chen³  Jing Liu³  Xiuli An¹  Jaime M. Ross² 

[1] Laboratory of Membrane Biology, New York Blood Center, New York, NY 10065, USA; E-Mail:State Key Laboratory of Medical Genetics & School of Life Sciences, Central South University, Changsha 410078, China;;State Key Laboratory of Medical Genetics & School of Life Sciences, Central South University, Changsha 410078, China; E-Mails:

关键词: autophagy;    modulators;    erythropoiesis;   

DOI  :  10.3390/ijms16024083

来源: mdpi

【 摘 要 】

Autophagy is a process that leads to the degradation of unnecessary or dysfunctional cellular components and long-lived protein aggregates. Erythropoiesis is a branch of hematopoietic differentiation by which mature red blood cells (RBCs) are generated from multi-potential hematopoietic stem cells (HSCs). Autophagy plays a critical role in the elimination of mitochondria, ribosomes and other organelles during erythroid terminal differentiation. Here, the modulators of autophagy that regulate erythroid differentiation were summarized, including autophagy-related (Atg) genes, the B-cell lymphoma 2 (Bcl-2) family member Bcl-2/adenovirus E1B 19 kDa interacting protein 3-like (Nix/Binp3L), transcription factors globin transcription factor 1 (GATA1) and forkhead box O3 (FoxO3), intermediary factor KRAB-associated protein1 (KAP1), and other modulators, such as focal adhesion kinase family-interacting protein of 200-kDa (FIP200), Ca²⁺ and 15-lipoxygenase. Understanding the modulators of autophagy in erythropoiesis will benefit the autophagy research field and facilitate the prevention and treatment of autophagy-related red blood cell disorders.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.