李英贤

发布者:马文君发布时间:2026-01-13浏览次数:31

联系方式

联系电话:13552722709

邮箱:yingxianli@aliyun.com

所在单位:中国航天员科研训练中心


个人简介

1989 9 - 1993 6 月:河北农业大学 学士

1993 9 - 1996 6 月:中国农业大学 硕士

2000 9 - 2003 6 月:军事医学科学院 细胞生物学 博士

1996 7 - 2005 10 月:航天医学工程研究所 助理研究员

2005 11 - 2007 10 月:美国杜克大学 博士后

2007 10 - 2012 10 月:中国航天员科研训练中心 副研究员

2012 10 - 至今:中国航天员科研训练中心 研究员

Personal Profile

1989.09-1993.06: Hebei Agricultural University Bachelor

1993.09-1996.06: China Agricultural University Master

2000.09-2003.06: Academy of Military Medical Sciences PhD in Cell Biology

1996.07-2005.10: Institute of Space Medicine & Medical Engineering Assistant Researcher

2005.11-2007.10: Duke University (USA) Postdoctoral Fellow

2007.10-2012.10: China Astronaut Research and Training Center Associate Professor

2012.10- : China Astronaut Research and Training Center Professor

 

研究方向和领域

空间生物学、生物医学工程

核心研究方向:航天失重生理效应对抗与防护(失重性骨丢失的发生机制及对抗防护;失重性心肌重塑的发生机制及对抗防护)

 

Research Directions and Fields

Space Biology, Biomedical Engineering 

Research Directions: Mechanisms and Countermeasures of Spaceflight-induced Physiological and Pathological Effects (Including Bone loss, cardiac remodeling, immunology dysfunction et al.)

研究内容 

针对航天特殊环境因素对机体的影响,尤其是“机体如何感应重力”这一航天医学领域的基本科学问题,在分子、细胞和组织器官等不同尺度上揭示重信号的感知、传导及调控机制,解析失重条件下机体不同组织的响应特征及其交互作用,为开发精准对抗防护策略、保障航天员在轨及返回后健康提供科学依据。

Research Interests 

Aiming at the impact of specific environmental factors in spaceflight on the human body, particularly the fundamental scientific question in aerospace medicine of how the body senses gravity, this research aims to uncover the mechanisms of gravitational signal perception, transmission, and regulation at various scales—molecular, cellular, and tissue/organ levels. It further seeks to analyze the response characteristics and interactions of different tissues in the body under gravitational conditions, thereby providing a scientific basis for developing precise countermeasures and protective strategies to safeguard astronauts' health during space missions and after their return.

研究成果 (最后通讯作者)

[1] Dynamic Changes in Hindlimb Motor Cortex Neurons during Simulated Weightlessness Revealed by Miniature 2-Photon Microscopy[J]. Research (Wash D C). 2025 Sep 19:8:0877.

[2] Precision-Arranged DNA Origami Plasmonic Nanoantennas for Multidimensional Smart-Warning of Weightlessness Induced Bone Loss. Adv Sci (Weinh). 2025 Aug 11:e07189.  doi: 10.1002/advs.202507189. 

[3] Tamsulosin ameliorates bone loss by inhibiting the release of Cl- through wedging into an allosteric site of TMEM16A Proc Natl Acad Sci [J]. 2025 Jan 7;122(1):e2407493121. 

[4]The mechanosensitive lncRNA Neat1 promotes osteoblast function through paraspeckle-dependent Smurf1 mRNA retention[J]. Bone Res, 2022, 10(1): 18. 

[5]Anoctamin 1 controls bone resorption by coupling Cl(-) channel activation with RANKL-RANK signaling transduction[J]. Nat Commun, 2022, 13(1): 2899. 

[6]Targeting E3 Ubiquitin Ligase WWP1 Prevents Cardiac Hypertrophy Through Destabilizing DVL2 via Inhibition of K27-Linked Ubiquitination[J]. Circulation, 2021, 144(9): 694-711. 

[7]3' untranslated region of Ckip-1 inhibits cardiac hypertrophy independently of its cognate protein[J]. Eur Heart J, 2021, 42(36): 3786-3799.

[8]TMCO1-mediated Ca(2+) leak underlies osteoblast functions via CaMKII signaling[J]. Nat Commun, 2019, 10(1): 1589.

[9]Lnc-mg is a long non-coding RNA that promotes myogenesis[J]. Nat Commun, 2017, 8(14718).

[10]Osteoclast-derived microRNA-containing exosomes selectively inhibit osteoblast activity[J]. Cell Discov, 2016, 2(16015). 

[11]miR-214 targets ATF4 to inhibit bone formation[J]. Nat Med, 2013, 19(1): 93-100. 

[12]CKIP-1 inhibits cardiac hypertrophy by regulating class II histone deacetylase phosphorylation through recruiting PP2A[J]. Circulation, 2012, 126(25): 3028-3040.