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Teresa C. Leone

Researcher at University of Pennsylvania

Publications -  53
Citations -  9092

Teresa C. Leone is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Peroxisome proliferator-activated receptor & Beta oxidation. The author has an hindex of 36, co-authored 51 publications receiving 8183 citations. Previous affiliations of Teresa C. Leone include University of Utah & Washington University in St. Louis.

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A critical role for the peroxisome proliferator-activated receptor alpha (PPARalpha) in the cellular fasting response: the PPARalpha-null mouse as a model of fatty acid oxidation disorders.

TL;DR: A critical role for PPAR alpha is defined in a transcriptional regulatory response to fasting and the PPARalpha-/- mouse is identified as a potentially useful murine model of inborn and acquired abnormalities of human fatty acid utilization.
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The cardiac phenotype induced by PPARα overexpression mimics that caused by diabetes mellitus

TL;DR: PPARalpha is a critical regulator of myocardial fatty acid uptake and utilization, activation of cardiac PPARalpha regulatory pathways results in a reciprocal repression of glucose uptake and usage pathways, and derangements in myocardian energy metabolism typical of the diabetic heart can become maladaptive, leading to cardiomyopathy.
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Lipin 1 is an inducible amplifier of the hepatic PGC-1α/PPARα regulatory pathway

TL;DR: It is demonstrated that the expression of lipin 1 is induced by peroxisome proliferator-activated receptor gamma (PPARgamma) coactivator 1alpha (PGC-1alpha), a transcriptional coactivators controlling several key hepatic metabolic pathways.
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Studying arrhythmogenic right ventricular dysplasia with patient-specific iPSCs

TL;DR: This study is the first to demonstrate that induction of adult-like metabolism has a critical role in establishing an adult-onset disease model using patient-specific iPSCs, and revealed crucial pathogenic insights that metabolic derangement in adult- like metabolic milieu underlies ARVD/C pathologies, enabling us to propose novel disease-modifying therapeutic strategies.