Editorial: Neutrophil extracellular traps: mechanistic and functional insight

Authors:
Open Access
Publisher website
Google Scholar
Abstract
Neutrophil extracellular traps: mechanistic and functional insight Neutrophil extracellular traps (NETs) have emerged as captivating elements within the complex realm of neutrophil biology. Originally renowned for their role in combating infections, neutrophils are now acknowledged for their diverse functions in immune responses and disease processes. NETs, consisting of DNA and proteins (1), effectively immobilize and eliminate pathogens, but their excessive release can trigger detrimental effects to the host (2). Various microbial and noninfectious stimuli have been identified to activate neutrophils and initiate NET formation (3). The production of reactive oxygen species (ROS) plays a crucial role in this process, with glutathionylation of actin and tubulin by the enzyme glutaredoxin 1 (Grx1) being essential for the active cytoskeleton movement required for NET release (4). Metabolic pathways, particularly glycolysis, are vital for the energy demands of neutrophils during NET formation (5). In addition to glycolysis, neutrophils also utilize the pentose-phosphate pathway (PPP) for NADPH and ribose production, and can adapt to fatty acid metabolism and glutaminolysis in certain conditions (6). NETs have been implicated in a pathogenesis of a wide range of diseases, including bacterial infections, autoimmune diseases, thrombosis, cancer, respiratory tract diseases, sepsis, cardiovascular diseases, inflammatory bowel diseases, neurodegenerative diseases, diabetic nephropathy, acute respiratory distress syndrome (ARDS), psoriasis, and COVID-19 (7). Though significant strides have been made in unraveling of NET formation, numerous inquiries and debates remain. Gaining deeper insights into the mechanisms and clinical implications of NET formation holds promise for the development of novel therapeutic interventions.

This publication has 12 references indexed in Scilit: