Chen Lab

Dr. Suet Nee Chen's lab is located within University of Colorado-Anschutz Medical Campus and the Department of Medicine-Division of Cardiology.

Her cutting edge laboratory focus on translational genomics research to define disease-causing gene mutations and to develop mechanism based treatment for inherited cardiomyopathy.   Dr. Chen's laboratory also develops and interrogates genetically engineered mouse models and CRISPR/Cas9 genome-edited human induced pluripotent stem cells to elucidate molecular mechanisms that cause the disease.

Major research projects focus on genetic contributions on intracellular signaling pathways, cell fate lineage tracing and identification of paracrine factors that mediate cross-talk between cardiac cells (cardiac myocytes, epicardial cells and fibroblasts) in the pathogenesis of dilated and arrhythmogenic cardiomyopathy.

Her highly motivated lab translates basic research discoveries into clinical treatment and diagnostics for genetic heart disease through collaborative interactions with the Mestroni and Taylor laboratories.   

Disease-Oriented Research Approach


Diesease oriented

Research



Molecular Mechanism Studies

Hippo_Model

 

Cell fate lineage tracing

Disease-Oriented Research Approach

Cross-talk between cardiac myocytes and non-cardiac myocytes

Crosstalk_cell typesv2

Lab Members


Suet Nee chen

Suet Chen Ph.D.

Asst Professor-Research
Department of Medicine-Division of Cardiology
Office Hours: 12700 E. 19th Ave. Aurora CO 80045 Room: P15-8006

Raffaella Lombardi M.D., Ph.D.

Associate Professor (Adjunct Professor)

Publications


Activation of PDGFRA signaling contributes to filamin C–related arrhythmogenic cardiomyopathy 

https://www.science.org/doi/10.1126/sciadv.abk0052?utm_source=rss&utm_medium=rss&utm_campaign=rss-sciadv

 

Established and Emerging Mechanisms in the Pathogenesis of Arrhythmogenic Cardiomyopathy: A Multifaceted Disease
Gao S, Puthenvedu D, Lombardi R, Chen SN. Established and Emerging Mechanisms in the Pathogenesis of Arrhythmogenic Cardiomyopathy: A Multifaceted Disease. Int J Mol Sci. 2020 Aug 31; 21(17). PMID: 32878278.

DNA Damage Response/TP53 Pathway Is Activated and Contributes to the Pathogenesis of Dilated Cardiomyopathy Associated With LMNA (Lamin A/C) Mutations
Chen SN, Lombardi R, Karmouch J, Tsai JY, Czernuszewicz G, Taylor MRG, Mestroni L, Coarfa C, Gurha P, Marian AJ. DNA Damage Response/TP53 Pathway Is Activated and Contributes to the Pathogenesis of Dilated Cardiomyopathy Associated With LMNA (Lamin A/C) Mutations. Circ Res. 2019 03 15; 124(6):856-873. PMID: 30696354.

The hippo pathway is activated and is a causal mechanism for adipogenesis in arrhythmogenic cardiomyopathy
Chen SN, Gurha P, Lombardi R, Ruggiero A, Willerson JT, Marian AJ. The hippo pathway is activated and is a causal mechanism for adipogenesis in arrhythmogenic cardiomyopathy. Circ Res. 2014 Jan 31; 114(3):454-68. PMID: 24276085.

Cardiology (SOM)

CU Anschutz

Anschutz Inpatient Pavilion 1

12605 East 16th Avenue

3rd Floor

Aurora, CO 80045


720-848-5300

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