We’re excited to share our latest publication in JACC: Basic to Translational Science, titled “Integrated Systems Biology Identifies Disruptions in Mitochondrial Function and Metabolism as Key Contributors to HFpEF.” This is a collaborative project with the Lefer Lab at Cedars-Sinai.

HFpEF, which accounts for ~50% of heart failure cases, is driven by profound disruptions in mitochondrial structure, function, and energy metabolism. Using the ZSF1-obese rat model, we found severe metabolic and transcriptional remodeling—marked by energy depletion, inflammation, and mitochondrial dysfunction—that underpin HFpEF progression. These findings highlight mitochondrial metabolism as a promising therapeutic target.