Dr. Arianne Caudal is a postdoctoral fellow at the Stanford Cardiovascular Institute with research interests in cardiac metabolism, disease modeling, and drug discovery. Dr. Caudal received her PhD in Biochemistry from the University of Washington, after conducting thesis work on mitochondrial metabolism and protein-protein interactions in the heart.
Honors & Awards
Postdoctoral Fellowship, American Heart Association (2022)
Postdoctoral Seed Grant, Cambridge Isotopes (2022)
TRAM Pilot Grant, Stanford University (2022)
SUMS Training Seed Award, Stanford University (2021)
Three Minute Thesis People's Choice Award, University of Washington (2021)
Predoctoral Fellowship, American Heart Association (2020-2022)
Doctor of Philosophy, University of Washington (2021)
Bachelor of Science, University of California Santa Barbara (2014)
Joseph Wu, Postdoctoral Faculty Sponsor
Mitochondrial interactome quantitation reveals structural changes in metabolic machinery in the failing murine heart.
Nature cardiovascular research
2022; 1 (9): 855-866
Advancements in cross-linking mass spectrometry (XL-MS) bridge the gap between purified systems and native tissue environments, allowing the detection of protein structural interactions in their native state. Here we use isobaric quantitative protein interaction reporter technology (iqPIR) to compare the mitochondria protein interactomes in healthy and hypertrophic murine hearts, 4 weeks post-transaortic constriction. The failing heart interactome includes 588 statistically significant cross-linked peptide pairs altered in the disease condition. We observed an increase in the assembly of ketone oxidation oligomers corresponding to an increase in ketone metabolic utilization; remodeling of NDUA4 interaction in Complex IV, likely contributing to impaired mitochondria respiration; and conformational enrichment of ADP/ATP carrier ADT1, which is non-functional for ADP/ATP translocation but likely possesses non-selective conductivity. Our application of quantitative cross-linking technology in cardiac tissue provides molecular-level insights into the complex mitochondria remodeling in heart failure while bringing forth new hypotheses for pathological mechanisms.
View details for DOI 10.1038/s44161-022-00127-4
View details for PubMedID 36405497
Generation of human induced pluripotent stem cell lines carrying heterozygous PLN mutation from dilated cardiomyopathy patients.
Stem cell research
2022; 63: 102855
Familial dilated cardiomyopathy (DCM) is among the most prevalent forms of inherited heart disease. Here, two human-induced pluripotent stem cell (iPSC) lines were generated from peripheral blood mononuclear cells (PBMCs) from DCM patients carrying different mutations in the phospholamban encoding-gene (PLN). Both iPSC lines exhibited normal morphology, karyotype, pluripotency marker expression, and differentiation into the three germ layers. These patient-specific iPSC lines serve as valuable in vitro models for DCM pathology caused by PLN mutations.
View details for DOI 10.1016/j.scr.2022.102855
View details for PubMedID 35853412
Human Induced Pluripotent Stem Cells for Studying Mitochondrial Diseases in the Heart.
Mitochondrial dysfunction is known to contribute to a range of diseases, and primary mitochondrial defects strongly impact high-energy organs such as the heart. Platforms for high-throughput and human-relevant assessment of mitochondrial diseases are currently lacking, hindering the development of targeted therapies. In the past decade, human induced pluripotent stem cells (iPSCs) have become a promising technology for drug discovery in basic and clinical research. In particular, human iPSC-derived cardiomyocytes (iPSC-CMs) offer a unique tool to study a wide range of mitochondrial functions and possess the potential to become a key translational asset for mitochondrial drug development. This review summarizes mitochondrial functions and recent therapeutic discoveries, advancements, and limitations of using iPSC-CMs to study mitochondrial diseases of the heart with an emphasis on cardiac applications.
View details for DOI 10.1002/1873-3468.14444
View details for PubMedID 35788991