Why the study?
Does overexpression of neutrophilic ACE alleviate glomerular injury in immune complex-mediated crescentic glomerulonephritis in mice?
Does overexpression of neutrophilic ACE alleviate glomerular injury in immune complex-mediated crescentic glomerulonephritis in mice?
Neutrophilic ACE provides renoprotection in immune complex-mediated crescentic glomerulonephritis via a complement C3-dependent mechanism requiring both C and N catalytic domains.
Hypothesis-generating for neutrophilic ACE in experimental GN; leaves open human translation and therapeutic targeting.
We recently reported that NeuACE mice that overexpress angiotensin-converting enzyme (ACE), specifically in neutrophils, alleviate glomerular injury in immune complex-mediated crescentic glomerulonephritis by the complement C3b-complement receptor 1/2 axis. Here, we showed that catalytically active C and N domains of ACE were needed for full renoprotection, and complement C3 was essential for the renoprotective role of overexpressed neutrophilic ACE. Furthermore, we highlighted the neutrophils' canonical pathogenic and noncanonical renoprotective functions via neutrophilic ACE through complement C3 in glomerulonephritis.
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Saito et al. (2025) studied this question.
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