Modelling arrhythmogenic cardiomyopathy fatty-fibro pathology with PKP2-deficient epicardial cells derived from human iPSCs
Communications Biology
We use patient-derived iPSC-cardiomyocytes, single-cell genomics, and computational approaches to understand cardiac disease mechanisms and identify therapeutic targets.
The Churko Lab at the University of Arizona integrates human iPSC technology with single-cell genomics, computational biology, and machine learning to understand the molecular basis of inherited cardiomyopathies. We develop new approaches for disease modeling, biomarker discovery, and therapeutic target identification.
Our foundation builds on methods pioneered at Stanford University in the laboratory of Dr. Joseph Wu, where we established approaches for iPSC-cardiomyocyte differentiation and high-throughput drug screening platforms that predict cardiotoxicity using patient-derived stem cells.
Dr. Jared Churko is an Associate Professor in the Department of Cellular and Molecular Medicine at the University of Arizona. He completed his postdoctoral training at Stanford University in the laboratory of Dr. Joseph Wu, where he developed methods for iPSC-cardiomyocyte differentiation and high-throughput cardiotoxicity screening. His research integrates human induced pluripotent stem cell technology with single-cell genomics and computational approaches to model inherited cardiac diseases, including arrhythmogenic cardiomyopathy, dilated cardiomyopathy, and atrial fibrillation. He serves on the editorial boards of JMCC Plus and Circulation: Heart Failure, and is a reviewer for NIH study sections.
Graduate Program Affiliations:
We combine stem cell biology, genomics, and computational methods to understand inherited cardiac diseases and identify new treatments.
We generate cardiomyocytes from patient blood to model inherited cardiac diseases including arrhythmogenic cardiomyopathy (PKP2, DSP), dilated cardiomyopathy (LMOD2, TTN), and atrial fibrillation. CRISPR/Cas9 isogenic controls enable precise genotype-phenotype analysis.
We use scRNA-seq to characterize cardiomyocyte heterogeneity during differentiation and identify disease-specific transcriptional signatures.
Integrating RNA-seq, proteomics (mass spectrometry), and whole-genome sequencing to identify disease biomarkers and therapeutic targets.
Engineering multicellular constructs with cardiomyocytes, fibroblasts, endothelial cells, and epicardial cells for physiologically relevant models.
From single-cell resolution to whole-genome analysis, our platforms generate deep biological insights.
Resolve cellular heterogeneity during cardiomyocyte differentiation. Identify rare cell populations and developmental trajectories at single-cell resolution.
Comprehensive transcriptomic and genomic profiling to identify disease signatures, variant effects, and pathway dysregulation.
Quantitative proteomics to measure protein abundance, post-translational modifications, and protein-protein interactions.
Multicellular constructs combining cardiomyocytes, endothelial cells, fibroblasts, and epicardial cells for physiologically relevant disease models.
Using single-cell RNA-sequencing, we map the transcriptional landscape of cardiomyocyte differentiation to understand how cells acquire atrial versus ventricular identity. This work reveals the molecular programs driving cardiac specification and identifies markers for isolating specific subpopulations.
We analyze patient-derived iPSC-cardiomyocytes using integrated multi-omics: whole-genome sequencing to identify variants, RNA-seq to measure transcriptional changes, and mass spectrometry to quantify protein alterations. This systems biology approach reveals disease mechanisms and therapeutic targets.
We engineer 3D cardiac tissues incorporating cardiomyocytes, fibroblasts, endothelial cells, and epicardial cells. These multicellular constructs better recapitulate the structural and functional properties of human myocardium, enabling more physiologically relevant disease modeling.
In collaboration with the Center for Innovations in Brain Sciences, we apply our iPSC expertise to generate disease-specific neural cells for neurodegenerative disease research.
Published > 50 articles | 6,299 citations | h-index 32 | NIH iCite Weighted RCR 132.90 | mean RCR 2.83
Communications Biology
Current Protocols
Circulation: Genomic and Precision Medicine
NPJ Regenerative Medicine
Nature Cardiovascular Research
Physiological Reports
Science Translational Medicine
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