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Cathepsin G in NETs activates complement C5, generating C5a, which enhances neutrophil NADPH oxidase activity through the C5aR1 receptor, establishing a prothrombotic-proinflammatory feedback loop (112, 113)

High-dose N-acetylcysteine therapy for novel H1N1 influenza pneumonia

doi: 10.5551/jat.RV17004 90 MooreKJTabasI

However, under pathological conditions, disease-specific Syn variants may engage in promiscuous, nonfunctional interactions with a broad spectrum of cellular proteins, burdening the cellular quality control machinery and potentially triggering neuronal cell death if left unchecked

doi: 10.1001/jama.2018.9511