Mouse models of pulmonary arterial hypertension exhibit significant anatomical, cellular, and genetic differences compared to rats, which may explain the varying degrees of pulmonary hypertension and vascular adaptation observed.
This review highlights the challenges and opportunities of using genetically engineered mice as models for pulmonary arterial hypertension research.
Many chronic pulmonary diseases are associated with pulmonary hypertension (PH) and pulmonary vascular remodeling, which is a term that continues to be used to describe a wide spectrum of vascular abnormalities. Pulmonary vascular structural changes frequently increase pulmonary vascular resistance, causing PH and right heart failure. Although rat models had been standard models of PH research, in more recent years the availability of genetically engineered mice has made this species attractive for many investigators. Here we review a large amount of data derived from experimental PH reports published since 1996. These studies using wild-type and genetically designed mice illustrate the challenges and opportunities provided by these models. Hemodynamic measurements are difficult to obtain in mice, and right heart failure has not been investigated in mice. Anatomical, cellular, and genetic differences distinguish mice and rats, and pharmacogenomics may explain the degree of PH and the particular mode of pulmonary vascular adaptation and also the response of the right ventricle.
Gomez‐Arroyo et al. (Sun,) conducted a review in Pulmonary arterial hypertension. Mouse models of pulmonary arterial hypertension exhibit significant anatomical, cellular, and genetic differences compared to rats, which may explain the varying degrees of pulmonary hypertension and vascular adaptation observed.