Key result
Chronically increased pulmonary lymph flow in an ovine model disrupted PPAR-γ signaling in lymphatic endothelial cells via KLF2, resulting in ROS accumulation and decreased bioavailable NO.
Population
Lymphatic endothelial cells isolated from the efferent vessel of the caudal mediastinal lymph node of…
Comparison
In vitro exposure to shear forces, transfection… vs Control LECs and baseline shunt LECs
Design
Preclinical
Authors
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May link PPAR-γ to lymphatic ROS/NO imbalance in CHD models; leaves open whether targeting it alters clinical outcomes.
Chronically elevated pulmonary lymph flow disrupts NO-mediated lymphatic function through KLF2-dependent PPAR-γ signaling, leading to ROS accumulation and decreased bioavailable NO.
Morris et al. (2018) studied Congenital heart disease with increased pulmonary blood flow (n=10). Chronically increased pulmonary lymph flow (shunt model) vs. Control (normal flow) was evaluated on KLF2 and PPAR-γ expression, ROS accumulation, and bioavailable NO in lymphatic endothelial cells. Chronically increased pulmonary lymph flow in an ovine model disrupted PPAR-γ signaling in lymphatic endothelial cells via KLF2, resulting in ROS accumulation and decreased bioavailable NO.