What is it about?
Beta arrestin 1 and 2 are ubiquitously expressed proteins that are best known as negative regulators of G protein signaling. Our findings reveal an additional isoform specific function of beta arrestin 1: it is required to sensitize soluble guanylyl cyclase (sGC) to nitric oxide (NO), enabling NO-dependent vasorelaxation in pulmonary arteries and maintaining normal blood pressure in the lung.
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Why is it important?
Reduced NO–mediated vasorelaxation in the pulmonary arteries elevates pulmonary arterial pressure, driving pulmonary hypertension (PH). This condition carries a poor prognosis and can progress to right heart failure, sometimes necessitating heart–lung transplantation. Thus, there is an urgent need to identify new molecular targets to enable the development of novel therapies.
Perspectives
The role of bArr1 in the pathophysiology of PH raises intriguing questions. Could a genetic mutation in PH patients affect beta arrestin 1 function? Future research may enable the development of a beta arrestin 1 activator, potentially paving the way for more effective treatments for PH.
Daniela Wenzel
Ruhr University Bochum
Read the Original
This page is a summary of: Beta arrestin 1 is a key regulator of pulmonary vascular tone, Proceedings of the National Academy of Sciences, February 2026, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2512602123.
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