Publications by authors named "Kyung-Seob Kim"

Controlling the microenvironment surrounding the pluripotent stem cells (PSCs) is a pivotal strategy for regulating cellular differentiation. Surface nanotopography is one of the key factors influencing the lineage-specific differentiation of PSCs. However, much of the underlying mechanism remains unknown.

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Direct cardiac reprogramming represents a novel therapeutic strategy to convert non-cardiac cells such as fibroblasts into cardiomyocytes (CMs). This process involves essential transcription factors, such as Mef2c, Gata4, Tbx5 (MGT), MESP1, and MYOCD (MGTMM). However, the small molecules responsible for inducing immature induced CMs (iCMs) and the signaling mechanisms driving their maturation remain elusive.

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The generation of mature and vascularized human pluripotent stem cell-derived cardiac organoids (hPSC-COs) is necessary to ensure the validity of drug screening and disease modeling. This study investigates the effects of cellular aggregate (CA) stemness and self-organization on the generation of mature and vascularized hPSC-COs and elucidates the mechanisms underlying cardiac organoid (CO) maturation and vascularization. COs derived from 2-day-old CAs with high stemness (H-COs) and COs derived from 5-day-old CAs with low stemness (L-COs) were generated in a self-organized microenvironment via Wnt signaling induction.

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Article Synopsis
  • Mature cardiomyocytes (CMs) derived from human pluripotent stem cells (hPSCs) are important for studying heart diseases and testing drugs more accurately.
  • The combination of FGF4 and ascorbic acid (AA) effectively promotes the differentiation of human embryonic stem cell-derived cardiogenic mesoderm cells into mature ventricular CMs.
  • FGF4+AA-treated CMs can release key biomarkers relevant to acute myocardial infarction and display gene expressions linked to coronary artery diseases when exposed to low oxygen levels, demonstrating their potential for in vitro hypoxic stress modeling.
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A novel tissue engineering strategy using 3D bio-print technology has become a promising therapeutic method for acute myocardial infarction (AMI) in an animal model. However, the application of 3D bio-printed tissue remains limited due to poor graft survival. Therefore, it is a scientific priority to enhance graft survival by precisely adjusting the 3D environment of encapsulated cells.

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