Reactive Oxygen and Nitrogen Species on Monocyte and Macrophage Biology

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are central regulators of monocyte and macrophage biology, shaping their survival, differentiation, migration, and effector functions. In monocytes and macrophages, ROS and RNS arise from endogenous sources, such as mitochondria, NADP...

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Detalles Bibliográficos
Autores: Jimenez Trinidad, Francisco Rafael|||0000-0002-5139-9774, Morini, Sofia|||0009-0006-8863-1975, Buffon, Armanda, de Prisco, Andrea, Galati, Greta, de Ciutiis, Astrid|||0000-0003-3434-500X, d'Aiello, Alessia|||0000-0003-3501-8684, Jiménez Altayó, Francesc|||0000-0002-9034-2041, Dantas, Ana Paula|||0000-0001-8514-4094, Liuzzo, Giovanna|||0000-0002-5714-0907, Severino, Anna
Tipo de recurso: artículo
Fecha de publicación:2026
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:dnet:uabarcelona_::f8a2b37496cdf617795a9b2b36e881f0
Acceso en línea:https://ddd.uab.cat/record/327829
https://dx.doi.org/urn:doi:10.3390/antiox15030389
Access Level:acceso abierto
Palabra clave:Oxidative stress
Reactive oxygen species
Reactive nitrogen species
Monocytes
Macrophages
Atherosclerosis
Descripción
Sumario:Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are central regulators of monocyte and macrophage biology, shaping their survival, differentiation, migration, and effector functions. In monocytes and macrophages, ROS and RNS arise from endogenous sources, such as mitochondria, NADPH oxidases, and myeloperoxidase, and from exogenous stimuli including pathogens, damaged tissues, and environmental oxidants. These reactive intermediates converge on redox-sensitive pathways such as NF-κB, Nrf2/HO-1, mitochondrial ROS signalling, and the NLRP3 inflammasome, thereby integrating metabolic stress with inflammatory activation. Redox balance is a key determinant of macrophage polarization: heightened ROS and RNS production drives pro-inflammatory M1 programs, whereas tightly regulated oxidative signalling supports M2 phenotypes associated with tissue repair and resolution. In chronic inflammatory disorders, notably atherosclerosis, oxidative stress amplifies monocyte recruitment, foam-cell formation, plaque instability, and maladaptive immunometabolic responses. The aim of this review is to recapitulate the major sources and functions of ROS and RNS in monocytes and macrophages and to synthesize current evidence on how these pathways collectively maintain or disrupt immune homeostasis. We further highlight emerging therapeutic strategies, such as NOX inhibitors, mitochondrial-targeted antioxidants, and Nrf2 activators, that seek to restore redox balance and offer promising avenues for the treatment of cardiovascular and immune-mediated diseases.