苗一非博士，HOPE裝置研究員，博士生導師。2012年畢業於北京大學醫學部基礎醫學八年製專業，獲病理生理學博士學位。之後於美國休斯頓大學、加州大學聖地亞哥分校、希望之城醫學中心從事博士後研究。2018年先後加入美國斯坦福大學和辛辛那提兒童醫院以講師、助理教授身份進行幹細胞以及類器官研究工作。期間領導並參與多項政府與企業資助的科研項目。2025年1月全職加入必威精装版app西汉姆联 參與人類器官生理病理模擬裝置（HOPE）建設，主要研究方向為利用胚胎幹細胞和誘導多能幹細胞分化的多種細胞和類器官模型，進行血管以及心肺係統的生理病生理體外模擬和疾病機製的探索。參與國家重點研發計劃項目和必威精装版app西汉姆联 自主部署項目。以第一作者或通訊作者身份（含共同）在 Cell, Circulation, Cell Stem Cell, Circulation Research, Nature Cardiovascular Research, Nature Communications, PNAS和ATVB等國際著名期刊上發表研究成果。長期擔任Cell Stem Cell, Circulation Research, ATVB, Communication Biology, Life Science, Metabolism: Clinical and Experimental等期刊獨立審稿人，Cell Proliferation雜誌青年編委。

類器官 (Organoids) 作為近年來生命科學領域的突破性技術，能夠高度模擬人體器官的三維結構、細胞組成及生理功能，為疾病建模、藥物篩選和再生醫學提供了革命性的研究工具。然而，類器官的研發麵臨諸多挑戰：例如，如何調控微環境以促進類器官的功能成熟，如何實現多種細胞類型的精準空間排布以模擬複雜的組織結構，以及如何實現高通量、標準化的生產以滿足研究和臨床應用的需求。為了解決這些問題，我們將遵循人體器官發育的基本原理，將人多能幹細胞在體外定向誘導分化為能夠精確模擬人體組織特異性血管間充質以的生理微環境，如血管化心、肺、肝髒、腦、腸道等類器官模型。並最終結合器官芯片以及3D生物打印技術，係統解析並重構多種複雜的器官三維結構與生理病生理功能，從而有針對性地、係統地搭建人體病理生理體外模擬係統，為器官再生提供基礎，並為新治療策略的探索提供新的研究方向。

（*第一作者,#通訊作者，含共同）

1. Miao Y*^#, Pek N*, Tan C*, Yu Z, Iwasawa K, Kechele DO, Sundaram N, Pastrana-Gomez V, Kishimoto K, Yang MC, Jiang C, Tchieu J, Whitsett JA, McCracken KW, Rottier RJ, Kotton DN, Helmrath MA, Wells JM, Takebe T, Zorn AM, Chen YW, Guo M^#, Gu M^#. Co-development of Mesoderm and Endoderm Enables Organotypic Vascularization in Lung and Gut Organoids. Cell. 2025 Aug.
2. Liu Z*, Liu Y*, Yu Z*, Pek N, ODonnell A, Glass I, Winlaw D, Guo M, Chen Y-W, Wu J, Yutzey K, Miao Y^#, Gu M^#. APOE-NOTCH Axis Governs Elastogenesis During Human Cardiac Valve Remodeling. Nature Cardiovascular Research. 2024 Aug;3(8):933-950
3. Dao L*, You Z*, Lu L*, Xu T*, Sarkar AK, Zhu H, Liu M, Calandrelli R, Yoshida G, Lin P, Miao Y, Mierke S, Kalva S, Zhu H, Gu M, Vadivelu S, Zhong S^#, Huang LF^#, Guo Z^#. Modeling blood-brain barrier formation and cerebral cavernous malformations in human PSC-derived organoids. Cell Stem Cell. 2024 Jun 6;31(6):818-833.
4. Yu Z*, Zhou X*, Liu Z, Pastrana-Gomez V, Liu Y, Guo M, Tian L, Nelson TJ, Wang N, Mital S, Chitayat D, Wu JC, Rabinovitch M, Wu SM, Snyder MP, Miao Y^#, Gu M^#. KMT2D-NOTCH Mediates Coronary Abnormalities in Hypoplastic Left Heart Syndrome. Circulation Research. 2022 Jul 22;131(3):280-282
5. Mikryukov AA*^#, Mazine A, Wei B, Yang D, Miao Y, Gu M, Keller GM^#. BMP10 Signaling Promotes the Development of Endocardial Cells from Human Pluripotent Stem Cell-Derived Cardiovascular Progenitors. Cell Stem Cell. 2021 Jan 7;28(1):96-111.
6. Miao Y*, Tian L*, Martin M, Paige SL, Galdos FX, Li J, Klein A, Zhang H, Ma N, Wei Y, Stewart M, Lee S, Moonen JR, Zhang B, Grossfeld P, Mital S, Chitayat D, Wu JC, Rabinovitch M, Nelson TJ, Nie S, Wu SM, Gu M^#. Intrinsic Endocardial Defects Contribute to Hypoplastic Left Heart Syndrome. Cell Stem Cell. 2020 Oct 1;27(4):574-589.
7. Paige SL*, Galdos FX*, Lee S*, Chin ET, Ranjbarvaziri S, Feyen DAM, Darsha AK, Xu S, Ryan JA, Beck AL, Qureshi MY, Miao Y, Gu M, Bernstein D, Nelson TJ, Mercola M, Rabinovitch M, Ashley EA, Parikh VN, Wu SM. Patient-Specific Induced Pluripotent Stem Cells Implicate Intrinsic Impaired Contractility in Hypoplastic Left Heart Syndrome. Circulation. 2020 Oct 20;142(16):1605-1608.
8. Tang X*, Miao Y*, Luo Y, Sriram K, Qi Z, Lin FM, Gu Y, Lai CH, Hsu CY, Peterson KL, Van Keuren-Jensen K, Fueger PT, Yeo GW, Natarajan R, Zhong S, Chen ZB^#. Suppression of Endothelial AGO1 Promotes Adipose Tissue Browning and Improves Metabolic Dysfunction. Circulation. 2020 Jul 28;142(4):365-379.
9. Miao Y*, Ajami NE*, Huang TS*, Lin FM, Lou CH, Wang YT, Li S, Kang J, Munkacsi H, Maurya MR, Gupta S, Chien S^#, Subramaniam S^#, Chen Z^#. Enhancer-associated long non-coding RNA LEENE regulates endothelial nitric oxide synthase and endothelial function. Nature Communications. 2018 Jan 18;9(1):292.
10. Miao Y*, Wu W, Dai Y, Maneix L, Huang B, Warner M, Gustafsson JÅ^#. Liver X receptor β controls thyroid hormone feedback in the brain and regulates browning of subcutaneous white adipose tissue. The Proceedings of the National Academy of Sciences, USA. 2015 Nov 10;112(45):14006-11.
11. Chen L*, Miao Y*, Zhang Y, Dou D, Liu L, Tian X, Yang G, Pu D, Zhang X, Kang J, Gao Y, Wang S, Breyer MD, Wang N, Zhu Y, Huang Y, Breyer RM, Guan Y^#. Inactivation of the E-prostanoid 3 receptor attenuates the angiotensin II pressor response via decreasing arterial contractility. Arteriosclerosis, Thrombosis, and Vascular Biology. 2012 Dec;32(12):3024-32.