title: [Receptor-interacting protein activation results in apoptosis, necroptosis and inflammation].
abstract: The receptor-interacting protein (RIP) has been identified to play a critical role in necroptosis, which is an inflammatory form of programmed necrosis in trauma, ischemia/reperfusion (I/R), and systemic inflammatory response syndrome (SIRS). Ripoptosome, a newly defined intracellular signaling complex with essential molecule of RIP1, can switch cell death mode between apoptosis and necroptosis. Based on molecular mechanism of RIP-dependent cell death and inflammation, with the understanding of the mechanisms of RIP-dependent apoptosis/necroptosis and its role in inflammation was summed up, and it was found that RIP plays a crucial role in regulating programmed cell death and inflammation. Therefore, further advances in understanding the mechanisms of necroptosis would be important in order to manipulate programmed cell death for therapeutic purposes in I/R injury, trauma, SIRS, and tumor.
authors.affiliation: Shanghai General Hospital of Nanjing Medical University, Shanghai 201620, China (Qian YB); Department of Critical Care Medicine, Shanghai General Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 201620, China (Qian YB, Wang RL). Corresponding author: Wang Ruilan, Email: wangyusun@hotmail.com.
authors.forename: Yongbing
authors.initials: Y
authors.lastname: Qian
authors.forename: Ruilan
authors.initials: R
authors.lastname: Wang
mesh_terms: D017209:Apoptosis; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D009336:Necrosis; D009369:Neoplasms / Q000503:physiopathology; D053422:Receptor-Interacting Protein Serine-Threonine Kinases / Q000502:physiology*; D015427:Reperfusion Injury / Q000503:physiopathology; D015398:Signal Transduction; D018746:Systemic Inflammatory Response Syndrome / Q000503:physiopathology; D014947:Wounds and Injuries / Q000503:physiopathology
chemical_list: C506249:RIPK1 protein, human; D053422:Receptor-Interacting Protein Serine-Threonine Kinases