Research Interests:

Organoids, a miniature organ, represent a revolutionary development in life sciences, closely mimicking the three-dimensional structures, cellular makeup, and physiological functions of human organs. They offer powerful tools for research in disease modeling, drug discovery, and regenerative medicine. Nevertheless, the advancement of organoids encounters several hurdles, such as optimizing the microenvironment to enhance functional maturation, achieving precise spatial arrangements of various cell types for complex tissue simulations, and ensuring high-throughput, standardized production for research and clinical needs. To tackle these challenges, we will adhere to the core principles of human organ development, guiding the differentiation of human pluripotent stem cells in vitro to accurately replicate the physiological microenvironment of tissue-specific vasculature and mesenchyme, including models of vascularized heart, lung, liver, brain, and intestine. By combining organ-on-a-chip and 3D bioprinting technologies, we will eventually reconstruct the three-dimensional structures and physiological functions of different complex organs. This approach will facilitate the targeted and systematic establishment of in vitro human pathophysiological simulation systems, laying the groundwork for organ regeneration and opening new avenues for innovative therapeutic strategies. In the past, we integrated multi-omics sequencing technologies with patient-derived induced pluripotent stem cells (iPSCs) to reconstruct various organ-specific vascular networks. This approach enabled us to identify tissue-specific vascular pathologies, investigate individualized disease mechanisms, and create new research avenues for developing potential therapeutic strategies for various congenital and degenerative cardiovascular diseases. 1). Uncover endothelium-centered mechanisms underlying single ventricle congenital heart defects (Cell Stem Cell, 2020; Circulation Research, 2022); 2). Construct the first high-resolution human fetal heart four-valve atlas to understand congenital valve hypoplasia (Nature Cardiovascular Research, 2024); 3). Recreate the authentic organotypic lung and intestine vascular bed via vascularized organoids (bioRxiv, 2024).

Awards and Honors:

2022, Guest Editor, Frontiers in Cardiovascular Medicine and Frontiers in Pediatric Cardiology; 2025 till now, Junior Editorial Board Member, Cell Proliferation. Peer Reviewer for: Circulation Research, ATVB, Communication Biology, Journal of Diabetes, Metabolism: Clinical and Experimental, etc.

Professional Activities:

Research Grants:

2024-2025, Initiative Scientific Research Program, Institute of Zoology, Chinese Academy of Sciences 2022-2023, LungMAP2 Pilot Award, NIH, USA, PI. 2017-2018, Postdoctoral fellowship, City of Hope Medical Center, USA, PI.

Selected Publications:

(*First author, #Coresponding author) 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 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#. Deciphering Endothelial and Mesenchymal Organ Specification in Vascularized Lung and Intestinal Organoids. bioRxiv. (2024). 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. 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 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. 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. 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. 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. 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. 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. 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.