Roles of TRAFs in Ischemia-Reperfusion Injury

Abstract

Tumor necrosis factor receptor-associated factor (TRAF) proteins are a family of signaling molecules that function downstream of multiple receptor signaling pathways, and they play a pivotal role in the regulation of intracellular biological progresses. These TRAFdependent signaling pathways and physiological functions have been involved in the occurrence and progression of ischemia-reperfusion injury (IRI), which is a common pathophysiological process that occurs in a wide variety of clinical events, including ischemic shock, organ transplantation, and thrombolytic therapy, resulting in a poor prognosis and high mortality. IRI occurs in multiple organs, including liver, kidney, heart, lung, brain, intestine, and retina. In recent years, mounting compelling evidence has confirmed that the genetic alterations of TRAFs can cause subversive phenotype changes during IRI of those organs. In this review, based on current knowledge, we summarized and analyzed the regulatory effect of TRAFs on the IRI of various organs, providing clear direction and a firm theoretical basis for the development of treatment strategies to manipulate TRAF proteins or TRAF-dependent signaling pathways in IRI-related diseases.

The role of necroptosis in common respiratory diseases in children

“…Then, when the reperfusion phase begins, the activated endothelial cells produce excessive amounts of ROS, which further cause oxidative stress and inflammatory damage, eventually leading to apoptosis, autophagy, and necrosis ( 19 ). It is currently believed that the mechanism of pulmonary parenchymal I/R injury is similar to that of reperfusion injury in other organs, a process that includes a significant increase in ROS, intracellular calcium influx, endothelial cell injury, complement system activation, and the release of inflammatory mediators such as tumor necrosis factor receptor-related factors ( 20 , 21 ). It has been shown that Nec-1 treatment significantly inhibits IR-induced necrotic cell death and the production of mitochondrial ROS ( 22 ).…”