Chia-Chi Key

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Assistant Professor

Wake Forest Baptist Medical Center

United States

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Dr. Chia-Chi Key is an Assistant Professor at Wake Forest Baptist Health in the United States. His research focuses on adipocyte differentiation, lipid metabolism, and the effects of inflammation on cellular signaling, as evident from his recent publications. He has investigated the roles of glucocorticoids, genetic factors influencing obesity, and innovative approaches in liquid biopsy techniques. Dr. Key's work integrates signaling and metabolism in various models, contributing to the understanding of metabolic diseases.

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ROLE OF HEPATIC GDPD3 IN MECHANISMS OF LIPID METABOLISM

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Articles (13)

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2025

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2022

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2022

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2021

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UNITED STATES

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Chia-Chi Key

Research Interests

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About

Recent Grants

Articles (13)

Muscle wasting and the response to exercise in lung-injured mice is not primarily driven through the glucocorticoid axis

GRK5 is required for adipocyte differentiation through ERK activation

Itaconate stabilizes CPT1a to enhance lipid utilization during inflammation

Itaconate stabilizes CPT1a to enhance lipid utilization during inflammation

Genetic Mapping of Multiple Traits Identifies Novel Genes for Adiposity, Lipids, and Insulin Secretory Capacity in Outbred Rats

Redox integration of signaling and metabolism in a head and neck cancer model of radiation resistance using COSM<sup>RO</sup>

ABHD4 regulates adipocyte differentiation in vitro but does not affect adipose tissue lipid metabolism in mice

A Liquid Biopsy-Based Approach to Isolate and Characterize Adipose Tissue-Derived Extracellular Vesicles from Blood

Genetic variation in satiety signaling and hypothalamic inflammation: merging fields for the study of obesity

<i>Keratinocyte-associated protein 3</i> plays a role in body weight and adiposity with differential effects in males and females.

Dichloroacetate reverses sepsis-induced hepatic metabolic dysfunction

Solute Carrier Family 37 Member 2 (SLC37A2) Negatively Regulates Murine Macrophage Inflammation by Controlling Glycolysis.

Human GDPD3 overexpression promotes liver steatosis by increasing lysophosphatidic acid production and fatty acid uptake

Collaborators (5)

Cristina M. Furdui

John Parks

Swapan Das

Gagan Deep

Anthony Molina

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