GLUTAMINOLYSIS: A DRIVER OF VASCULAR AND CARDIAC REMODELING IN PULMONARY ARTERIAL HYPERTENSION

Glutaminolysis: A Driver of Vascular and Cardiac Remodeling in Pulmonary Arterial Hypertension

Glutaminolysis: A Driver of Vascular and Cardiac Remodeling in Pulmonary Arterial Hypertension

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Pulmonary arterial hypertension (PAH) is a decimating ailment described by chronic precapillary pulmonary hypertension, an elevated mean pulmonary arterial pressure with a normal pulmonary capillary wedge pressure, and a raised pulmonary vascular resistance resulting in increased right ventricular afterload culminating in satisfyer pro penguin next generation heart failure and death.Current PAH treatments regulate the vasodilatory/vasoconstrictory balance of pulmonary vessels.However, these treatment options are unable to stop the progression of, or reverse, an already established disease.Recent studies have advanced a metabolic dysregulation, featuring increased glutamine metabolism, as a mechanism driving PAH progression.Metabolic dysregulation in PAH leads to increased glutaminolysis to produce substrate to meet the high-energy requirement lock shock and barrel art by hyperproliferative and apoptosis-resistant pulmonary vascular cells.

This article explores the role of glutamate metabolism in PAH and how it could be targeted as an anti-remodeling therapeutic strategy.

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