NUS Graduate School for Integrative Sciences and Engineering

Roger FOO

Research Areas
Brief Description of Research
1. Cardiovascular Biology
2. Stem Cell Biology & Regenerative Medicine
3. Molecular Genomics


Heart failure (HF) is a leading cause of mortality and morbidity, and a huge healthcare burden in modern society. Treatment for HF remains an inadequate stage-by-stage cumulative add-on therapy, and prognosis threatens to worsen as the world population is rapidly aging. Novel targets are urgently needed for the HF drug discovery pipeline.

An underlying defect in HF patients is the progressive loss of cardiomyocytes (CMs), accompanied by functional derangements in contraction and relaxation. The regenerative capacity of the heart is limited by the inability of terminally differentiated CMs to adequately undergo cell division after the first weeks of life. However, recent studies have found that very low rate of cardiomyocyte turnover occurs in adult mouse and human hearts, mediated primarily by proliferation of pre-existing CMs. The evidence of human CM renewal suggests that the development of pharmacological strategies to stimulate this process may be a rational approach itself, or complement to cell transplantation strategies for CM replacement. Therefore, it is important to uncover gene regulatory pathways/drivers mediating the proliferation of pre-existing CMs in normal and failing human hearts.

In order to tackle the important question, we will employ cutting edge technologies including single cell RNA-seq, live cell imaging, high-throughput content screening, CRISPR genome editing, and engineered heart tissue in both mouse and human models. Our project aims to:

  1. profile genome-wide transcriptome of single cell healthy and diseased cardiomyocytes from mouse and human hearts,
  2. discover unique and evolutionary conserved gene regulatory pathways specific for distinct subsets of cardiomyocytes relevant to cardiac regenerative potential,
  3. functionally validate selected candidates to induce the proliferation of pre-existing cardiomyocytes.