The Szweda Laboratory studies how nutrient and energetic stress alter cardiac metabolism and contribute to heart disease. Its work centers on the idea that the healthy heart must continually adjust how it uses glucose and fatty acids in response to changing physiologic demands, and that loss of this metabolic flexibility can drive cardiovascular dysfunction.
The laboratory investigates how mitochondrial metabolism, redox signaling and fuel selection are regulated in the heart during obesity, diabetes, hypertension, aging and other forms of stress. By defining the molecular mechanisms that connect metabolism to cardiac performance, the lab aims to identify metabolic determinants of heart disease and pathways that can be targeted to promote heart health.
Research Themes
Cardiac Metabolic Flexibility
Understanding how the heart switches between glucose and fatty acid oxidation in response to changes in nutrient availability, workload and physiologic demand.
Mitochondrial Function and Redox Biology
Investigating how oxidative stress, redox-dependent signaling and mitochondrial injury alter cardiac bioenergetics and contribute to disease progression.
Nutrient Stress, Aging and Heart Disease
Defining how obesity, diabetes, aging and related metabolic stressors reshape myocardial metabolism and increase vulnerability to cardiovascular disease.
Metabolic Determinants of Cardiac Injury and Recovery
Identifying molecular pathways that regulate fuel use, mitochondrial resilience and cardiac adaptation in ways that may lead to new therapeutic strategies.
Selected Publications
This study demonstrated that mitochondrial fuel utilization plays a key role in regulating cardiomyocyte proliferation. The findings link cardiac metabolism directly to cell cycle control and provide new insight into how metabolic pathways influence heart regeneration.
This landmark study showed that exposure to the oxygen-rich postnatal environment activates DNA damage signaling that halts cardiomyocyte proliferation, providing a mechanistic explanation for why the mammalian heart rapidly loses regenerative capacity after birth.
A comprehensive list of publications from the Szweda Laboratory is available on PubMed.
