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Chronic pulmonary hypertension (CPH) is a debilitating disorder that remains one of the most vexing, life-threatening clinical problems in cardiopulmonary medicine. While CPH is a disease process that often originates in the lungs, it is the downstream consequences that produce right heart failure and death in the majority of patients. As such, understanding the differential cellular response to CPH within the right atrium and ventricle is paramount for developing guided molecular interventions. Such therapy is needed to arrest the negative metabolic perturbations that are the direct consequence of prolonged pressure overload.
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