SH Cheng - Life Science and Medicine

28

37

32.5

Zheng Yi Tay

Mr

28/08/2001

A5642

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+85254219133

6T, 6/F, KIU YU MANSION 86 LOK SHAN ROAD
TO KWA WAN, KOWLOON
Hong Kong

I am thrilled to apply for the Hong Kong Laureate Forum as a researcher in the stem cell field, focusing on cardiac diseases. My work aims to develop innovative therapies for heart-related conditions, and I am inspired by the opportunity to learn from laureates whose groundbreaking discoveries have shaped modern science. Their insights will deepen my understanding of stem cell applications and guide me in addressing critical challenges in cardiac regeneration.

The forum’s interdisciplinary environment is ideal for exploring new perspectives and fostering collaborations. I am particularly interested in discussing how stem cell research can be integrated with other fields to advance treatments for heart disease, a leading cause of global mortality. Engaging with experts and peers will help me refine my research approach and contribute to transformative solutions.

Beyond the lab, I am passionate about science communication and education. The forum’s mission to inspire future scientists aligns with my goal of making stem cell research accessible and impactful. I hope to bring back valuable knowledge and connections to share with my community and inspire the next generation of researchers.

Joining the Hong Kong Laureate Forum is a unique opportunity to grow as a scientist and collaborator. I am eager

Postgraduate (PhD)

Biomedical Sciences

The University of Hong Kong

Hong Kong, China

HKU Presidential PhD Scholar Programme

Cardiac fibrosis is a major driver of heart failure progression, yet therapeutic options remain limited. Signal transducer and activator of transcription 3 (STAT3), a key transcription factor, plays a pivotal role in fibrosis by promoting fibroblast activation and extracellular matrix deposition. In this study, we explore the use of base editing, a precise genome-editing technology, to introduce targeted mutations in the STAT3 gene, aiming to disrupt its pro-fibrotic functions. We have established an in vitro model using fibroblasts cell lines treated with TGF-β1 to induce fibrotic differentiation. Using a lentiviral vector, we delivered a cytosine base editor targeting the STAT3 gene to these cells. Preliminary data show reduced expression of fibrosis markers (α-SMA and collagen I) in edited cells compared to controls. Building on these findings, future work will employ stem cell-derived cardiac organoids to model fibrosis in a 3D multicellular system that recapitulates human cardiac pathophysiology.

Leveraging high-throughput base editing screening, we aimed to identify specific STAT3 mutations that effectively inhibit fibrotic pathways in cardiac fibroblasts and develop a precision therapy that not only halts fibrosis progression but also preserves cardiac function.