title: Autophagy as a regulatory component of erythropoiesis.
abstract: 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.
authors.affiliation: State Key Laboratory of Medical Genetics & School of Life Sciences, Central South University, Changsha 410078, China. jzhang@nybloodcenter.org.|Red Cell Physiology Laboratory, New York Blood Center, New York, NY 10065, USA. jzhang@nybloodcenter.org.
authors.forename: Jieying
authors.initials: J
authors.lastname: Zhang
authors.affiliation: State Key Laboratory of Medical Genetics & School of Life Sciences, Central South University, Changsha 410078, China. wukunlu@163.com.
authors.forename: Kunlu
authors.initials: K
authors.lastname: Wu
authors.affiliation: State Key Laboratory of Medical Genetics & School of Life Sciences, Central South University, Changsha 410078, China. xiaojuan_xiao0809@163.com.
authors.forename: Xiaojuan
authors.initials: X
authors.lastname: Xiao
authors.affiliation: State Key Laboratory of Medical Genetics & School of Life Sciences, Central South University, Changsha 410078, China. liaojilingcsu@163.com.
authors.forename: Jiling
authors.initials: J
authors.lastname: Liao
authors.affiliation: State Key Laboratory of Medical Genetics & School of Life Sciences, Central South University, Changsha 410078, China. huqikang1001@163.com.
authors.forename: Qikang
authors.initials: Q
authors.lastname: Hu
authors.affiliation: State Key Laboratory of Medical Genetics & School of Life Sciences, Central South University, Changsha 410078, China. chenhy5000@126.com.
authors.forename: Huiyong
authors.initials: H
authors.lastname: Chen
authors.affiliation: State Key Laboratory of Medical Genetics & School of Life Sciences, Central South University, Changsha 410078, China. liaojilingcsu@163.com.
authors.forename: Jing
authors.initials: J
authors.lastname: Liu
authors.affiliation: Laboratory of Membrane Biology, New York Blood Center, New York, NY 10065, USA. xan@nybloodcenter.org.|College of Life Science, Zhengzhou University, Zhengzhou 450001, China. xan@nybloodcenter.org.
authors.forename: Xiuli
authors.initials: X
authors.lastname: An
mesh_terms: D001093:Arachidonate 15-Lipoxygenase / Q000378:metabolism; D001343:Autophagy; D004912:Erythrocytes / Q000166:cytology / Q000378:metabolism; D004920:Erythropoiesis; D006412:Hematopoietic Stem Cells / Q000166:cytology; D006801:Humans; D011505:Protein-Tyrosine Kinases / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism; D017086:beta-Thalassemia / Q000378:metabolism / Q000473:pathology
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D014157:Transcription Factors; D001093:Arachidonate 15-Lipoxygenase; D011505:Protein-Tyrosine Kinases