Metabolic Syndrome–Associated Pulmonary Hypertension: Role ofEndothelin-1 and Inflammatory Signaling in a High-Fat Diet Model

Authors: Adrian Chimbo, Melinee D’Silva , Christina Signoretti1 , Ashley Linton-Edwards , and Sachin A. Gupte

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This poster presentation, co-authored by Adrian Chimbo and colleagues, investigates the underlying mechanisms linking metabolic syndrome to an increased risk of pulmonary arterial hypertension (PAH) using a high-fat diet (HFD) rat model. The study demonstrates that rats fed an HFD exhibit altered pulmonary function, characterized by a decreased pulmonary artery acceleration time to ejection time (PAAT/ET) ratio, increased peak velocity, and increased arterial wall thickness.

Furthermore, the research connects these physiological changes to inflammatory and vasoconstrictive signaling pathways, showing a significant upregulation of pro-inflammatory chemokines like CCL2 and CCL7, an elevation of the vasoconstrictor metabolite 12(S)-HETE, and a downregulation of anti-inflammatory fatty acids and oxylipins. Ultimately, the findings suggest that a high-fat diet drives pulmonary hypertension by triggering endothelin-1 activation and pro-inflammatory cytokine expression, with future research aims directed toward examining group 3 PAH under prolonged hypoxia