We study the role of stress responses in aging and age-related diseases.

Research in the Kim lab focuses on the role of mitochondrial-mediated, cross-compartmental communication in the maintenance of cellular homeostasis. Using cutting-edge technologies in C. elegans genetics, mouse genetics, molecular biology, and biochemistry, we aim to understand the connection between mitochondrial metabolism, aging, and age-related diseases.


Proposed mechanism of Mitochondrial-to-Cytosolic Stress Response (MCSR) regulation; mtHSP70 reduction or CPT inhibitor PHX can serve as UPRmt inducers and shift the fat metabolism pathway to the fat storage pathway. Stressed mitochondria (shown in pink) would alter fatty acid metabolism. Changes in lipid balance may serve as a cytosolic signal to turn on the cytosolic response to improve cytosolic protein homeostasis. In this, cardiolipin serves as an activator of the MCSR by reducing the level of an MCSR inhibitor, ceramide. DVE-1 and HSF-1 seem to cooperate to induce the cytosolic response upon mitochondrial perturbation.

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