Nalazite se na CroRIS probnoj okolini. Ovdje evidentirani podaci neće biti pohranjeni u Informacijskom sustavu znanosti RH. Ako je ovo greška, CroRIS produkcijskoj okolini moguće je pristupi putem poveznice www.croris.hr
izvor podataka: crosbi

Pathophysiology of neutrophil-mediated extracellular redox reactions (CROSBI ID 226450)

Prilog u časopisu | pregledni rad (znanstveni) | međunarodna recenzija

Jaganjac, Morana ; Čipak, Ana ; Schaur, Rudolf J. ; Žarković, Neven Pathophysiology of neutrophil-mediated extracellular redox reactions // Frontiers in bioscience, 21 (2016), 839-855. doi: 10.2741/4423

Podaci o odgovornosti

Jaganjac, Morana ; Čipak, Ana ; Schaur, Rudolf J. ; Žarković, Neven

engleski

Pathophysiology of neutrophil-mediated extracellular redox reactions

Neutrophil granulocyte leukocytes (neutrophils) play fundamental role in the innate immune response. In the presence of adequate stimuli, neutrophils release excessive amount of reactive oxygen species (ROS) that may induce cell and tissue injury. Oxidative burst of neutrophils acts as a double-edged sword. It may contribute to the pathology of atherosclerosis and brain injury but is also necessary in resolving infections. Moreover, neutrophil-derived ROS may also have both a tumor promoting and tumor suppressing role. ROS have a specific activities and diffusion distance, which is related to their short lifetime. Therefore, the manner in which ROS will act depends on the cells targeted and the intra- and extracellular levels of individual ROS, which can further cause production of reactive aldehydes like 4-hydroxynonenal (HNE) that act as a second messengers of ROS. In this review we discuss the influence of neutrophil mediated extracellular redox reactions in ischemia reperfusion injury, transplant rejection and chronic diseases (atherosclerosis, inflammatory bowel diseases and cancer). At the end a brief overview of cellular mechanisms to maintain ROS homeostasis is given.

neutrophils ; reactive oxygen species ; oxidative burst ; 4-hydroxynonenal ; ischemia reperfusion injury ; transplant rejection and chronic diseases

nije evidentirano

nije evidentirano

nije evidentirano

nije evidentirano

nije evidentirano

nije evidentirano

Podaci o izdanju

21

2016.

839-855

objavljeno

1093-9946

10.2741/4423

Povezanost rada

nije evidentirano

Poveznice
Indeksiranost