Key result
Hypertension and biological sex alter lung RAS by reducing ACE2, heightening susceptibility to pulmonary injury.
Why the study?
Emerging evidence suggests hypertension and biological sex shape lung renin-angiotensin system signaling and susceptibility to lung injury, but these mechanisms and potential therapeutic strategies needed synthesis.
Design
Mini-review
Alerts clinicians to heightened lung injury risk in hypertensive patients by sex; leaves open need for prospective validation.
The pulmonary renin-angiotensin system (RAS) is a key regulator of endothelial function, inflammation, and tissue remodeling. Emerging evidence indicates that both hypertension and biological sex shape lung RAS signaling by shifting the balance between the ACE/Ang II/AT1R and ACE2/Ang-(1–7)/Mas pathways. This imbalance promotes oxidative stress, inflammatory activation, and fibrotic remodeling, increasing susceptibility to lung injury. Experimental and clinical data show that hypertension is associated with reduced pulmonary ACE2 activity and enhanced pro-inflammatory signaling, while sex-dependent differences further modulate lung RAS composition and disease vulnerability. These mechanisms may predispose the lungs to exaggerated responses to secondary insults, including acute lung injury, respiratory distress syndromes, and viral infections such as COVID-19. This mini-review summarizes current evidence linking hypertension- and sex-dependent lung RAS dysregulation to pulmonary injury and highlights therapeutic strategies aimed at restoring local RAS balance.
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Ribeiro-Silva et al. (2026) studied this question. Hypertension and biological sex alter lung RAS by reducing ACE2 and increasing pro-inflammatory signaling, heightening susceptibility to pulmonary injury and lung disease.
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