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Chronic pulmonary hypertension (CPH) is a devastating syndrome that rests as one of the most worrying, deadly clinical problems in cardiopulmonary medicine. Although CPH is a disease progression that frequently initiates in the lungs, it is the downstream penalties that yield right heart failure and death in the majority of patients. As such, considerate the differential cellular response to CPH within the right atrium and ventricle is supreme for evolving guided molecular interventions. Such therapy is required to stop the negative metabolic agitations that are the direct import of prolonged pressure overload.
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