Key result
Sustained abnormal CD39 activity in the pulmonary vasculature results in ATP accumulation and adenosine diminution, promoting the vasoconstriction and vascular remodeling seen in pulmonary arterial hypertension.
Why the study?
Current therapies for pulmonary arterial hypertension fail to impact long-term outcomes, and targeting the regulation of ATP and adenosine via CD39 may offer a novel therapeutic pathway.
CD39 and adenosine signaling pathways represent potential novel therapeutic targets for pulmonary arterial hypertension by modulating endothelial dysfunction and vascular remodeling.
CD39 targeting should not yet change PAH practice; leaves open whether it reverses vascular remodeling.
Pulmonary arterial hypertension (PAH) is a devastating progressive disease characterised by pulmonary arterial vasoconstriction and vascular remodelling. Endothelial dysfunction has emerged as a contributing factor in the development of PAH. However, despite progress in the understanding of the pathophysiology of this disease, current therapies fail to impact upon long-term outcomes which remain poor in most patients. Recent observations have suggested the disturbances in the balance between ATP and adenosine may be integral to the vascular remodelling seen in PAH. CD39 is an enzyme important in regulating these nucleos(t)ides which may also provide a novel pathway to target for future therapies. This review summarises the role of adenosine signalling in the development and progression of PAH and highlights the therapeutic potential of CD39 for treatment of PAH.
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Willcox et al. (2022) conducted a review in Pulmonary arterial hypertension. CD39 was evaluated. Sustained abnormal CD39 activity in the pulmonary vasculature results in ATP accumulation and adenosine diminution, promoting the vasoconstriction and vascular remodeling seen in pulmonary arterial hypertension.
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