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Song Lab

Cardiomyogenesis, Human Heart Disease, and Regenerative Medicine

The heart is the first functional organ formed in mammals. Ischemic heart disease resulting in myocardial infarction (MI) and heart failure is the leading cause of morbidity and mortality. A fundamental process leading to heart failure post-MI is irreversible loss of cardiomyocytes, which are replaced by fibrotic scar tissue that impairs the pump function of the heart. The long-term goal of research in our lab is to develop potential therapeutic strategies for heart disease. In addition to our robust internal research programs, we actively collaborate with others in the field with the long term goal of promoting the use of regenerative medicine to improve human health. 

1. Molecular mechanisms for decisions of cardiomyocyte fate.

Terminally differentiated fibroblasts and pluripotent stem cells can transdifferentiate or differentiate into cardiomyocytes. We attempt to unravel mechanisms underlying determination of cardiomyocyte fate, and use mutant mouse models to dissect signaling pathways governing heart development.


2. Laboratory models of human heart disease.

We unravel molecular mechanisms for development of heart disease and search for potential cures by using induced pluripotent stem cells (iPS cells) derived from heart disease patients.

  •  alt=



  •  alt=Kunhua Song

    Assistant Professor of Medicine,
    Divison of Cardiology,
    Charles C. Gates Center for Regenerative Medicine and Stem Cell Biology,
    Training Faculty:
    - Molecular and Cellular Pharmacology Graduate Program
    - Cell Biology, Stem Cells and Development Graduate Program

Postdoctoral Researcher

  •  alt=Yuanbiao Zhao

    B.S. - Wuhan University, Wuhan
    Ph.D. - China Agricultural University, Beijing
    Interests: Cardiomyogenesis and regenerative medicine


  •  alt=Andrew Riching

    B.S. - University of Wisconsin-Madison
    Ph.D. candidate in Molecular and Cellular Pharmacology Program
    Interests: Epigenetic regulation of cardiomyogenesis, translational research and regenerative medicine

Research Assistants

  •  alt=Pilar Londono

    B.S. - Metropolitan State University of Denver
    M.S. University of Colorado - Denver
    Interests: Stem cell biology, regenerative medicine for cardiovascular disease.
  • Yingqiong Cao

    B.S. - Dalian University of Technology, Dalian
    M.S. - China Agricultural University, Beijing
    Interests: Molecular mechanisms and laboratory models of human heart disease.

Boettcher Scholar

  •  alt=Ellis Aune

    University of Colorado-Boulder, class of 2018
    Interests: Human stem cell biology, electrophysiology, biochemistry, molecular engineering for heart disease.

1. Zhao Y, Londono P, Cao Y, Sharpe EJ, Proenza C, O’Rourke R, Jones KL, Jeong MY, Walker LA, Buttrick PM, McKinsey TA, and Song K. (2015) High-efficiency reprogramming of fibroblasts into cardiomyocytes requires suppression of pro-fibrotic signaling.​ Nature Communications, 6: 8243.

2. Du Bois P, Pablo Tortola C, Lodka D, Kny M, Schmidt F, Song K, Schmidt S, Bassel-Duby R, Olson EN, Fielitz J. (2015) Angiotensin II Induces Skeletal Muscle Atrophy by Activating TFEB-Mediated MuRF1 Expression. Circulation Research 117: 424-36.

Before 2015
1. Long C*, Grueter CE*, Song K*, Qin S, Qi X, Kong YM, Shelton JM, Richardson JA, Zhang CL, Bassel-Duby R, and Olson EN. (2014) Ataxia and Purkinje cell degeneration in mice lacking the CAMTA1 transcription factor. Proc Natl Acad Sci U S A. 111: 11521-6. (*These authors contributed equally to the work).

2. Nam YJ, Song K, Luo X, Daniel E, Lambeth K, West K, Hill JA, DiMaio JM, Baker LA, Bassel-Duby R, and Olson EN. (2013) Reprogramming of human fibroblasts toward a cardiac fate. Proc Natl Acad Sci U S A. 110, 5588-93.

3. Nam YJ, Song K, and Olson EN. (2013) Heart repair by cardiac reprogramming. Nature Medicine 19, 413-5.

4. Song K, Nam YJ, Luo X, Qi X, Tan W, Huang GN, Acharya A, Smith CL, Tallquist MD, Neilson EG, Hill JA, Bassel-Duby R, and Olson EN. (2012) Heart repair by reprogramming non-myocytes with cardiac transcription factors.​ Nature 485, 599-604.

5. Backs J, Song K, Bezprozvannaya S, Chang S, and Olson EN. (2006) CaM kinase II selectively signals to histone deacetylase 4 during cardiomyocyte hypertrophy. Journal of Clinical Investigation, 116, 1853-64.

6. Song K, Backs J, McAnally J, Qi X, Gerard RD, Richardson JA, Hill JA, Bassel-Duby R, and Olson EN. (2006). The transcriptional coactivator CAMTA2 stimulates cardiac growth by opposing class II histone deacetylases.​ Cell, 125(3):453-66. ​​

Kunhua Song, Ph.D.
Division of Cardiology, Department of Medicine
Charles C. Gates Center for Regenerative Medicine and Stem Cell Biology
University of Colorado Anschutz Medical Campus
12700 E. 19th Ave B-139
Aurora, CO 80045
Phone: (303) 724-8132
Fax: (303) 724-5450 ​​