Current Projects

How does a mother's metabolic health shape her child's lifelong health?

The Maloyan Laboratory studies how maternal obesity and metabolic disease during pregnancy affect the development and long-term health of offspring. We combine experimental models, human biospecimens, physiological assessments, and molecular profiling to uncover the mechanisms that link the early developmental environment to cardiovascular, metabolic, immune, and pulmonary health. A central question across our work is why male and female offspring respond differently to these exposures.

1. How do early-life exposures shape the heart and blood vessels in adulthood?

We investigate how maternal obesity alters cardiac development, blood pressure, and vascular function in offspring. In experimental models, male and female offspring respond differently: males are more susceptible to hypertension, cardiac hypertrophy, and fibrosis. We are examining how changes in epigenetic regulation, gene expression, and cellular responses to mechanical stress drive these outcomes. By integrating molecular studies with cardiovascular imaging and physiological measurements, we aim to identify the pathways that promote disease and those that confer resilience.

2. Does maternal obesity leave a lasting imprint on the immune system?

Immune cells depend on specific metabolic pathways to function. We are testing whether maternal obesity reprograms these pathways during development, producing lasting changes in immune cell behavior that contribute to inflammation and metabolic disease. Using bone marrow transplantation, cellular metabolic profiling, and studies of human cord blood, we examine how developmental exposures affect myeloid cells and their interactions with other tissues. Our goal is to define how immune cell metabolism influences offspring health and to determine whether these changes can be reversed.

3. How does the placenta respond to maternal obesity, and why does the response differ by fetal sex?

The placenta controls the exchange of nutrients and signals between mother and fetus. Our work centers on dipeptidyl peptidase 4 (DPP4), a protein involved in metabolic and inflammatory signaling that is elevated in male placentas from pregnancies complicated by obesity. We are investigating how DPP4 affects mitochondrial function and lipid metabolism in trophoblasts, how microRNA regulation contributes to differences between male and female placentas, and how maternal immune cells influence placental function. By analyzing maternal blood across pregnancy alongside placental and cord blood samples, we aim to connect these mechanisms to the environment the fetus experiences.

4. How does the maternal metabolic environment affect lung health?

We study how maternal obesity influences lung development and respiratory function in offspring, with a focus on histone deacetylase 9 (HDAC9), a regulator of gene expression in alveolar epithelial cells. Combining respiratory physiology, lipid profiling, and cell-specific genetic approaches, we investigate how altered gene regulation, lipid metabolism, and cellular senescence contribute to lung dysfunction, and whether these mechanisms differ between males and females.

5. Toward prevention

Across these projects, our long-term goal is to identify biological pathways that can guide strategies to improve maternal and child health. By learning when developmental changes arise and which mechanisms remain modifiable, we aim to lay the groundwork for interventions that reduce disease risk across generations

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