[Programmed necrosis: a new target for ischemia reperfusion injury].
Recent years, the researchers have found a new type of cell death, referred to programmed necrosis or necroptosis, which involves the death receptor and the ligand binds and is initiated under the inhibition of apoptosis pathway. Programmed necrosis possesses the morphological features of typical necrosis accompanied by inflammation. The receptor interacting protein kinase 1/3(RIPK1/3) can be inhibited by the specific inhibitors, such as necrostatin-1. RIPK1/3 could regulate programmed necrosis and play a key role in the process. The significance of programmed necrosis in ischemia-reperfusion injury (IRI) has been attracted great attention at present. Simultaneously, a series of studies have found it also involves in the IRI of heart, kidney, brain and retina.
Research Center of National Health Ministry on Transplantation Medicine Engineering and Technology, Third Xiangya Hospital, Central South University, Changsha 410013, China.
Xiaojing
X
Li
Research Center of National Health Ministry on Transplantation Medicine Engineering and Technology, Third Xiangya Hospital, Central South University, Changsha 410013, China.
Yingzi
Y
Ming
Research Center of National Health Ministry on Transplantation Medicine Engineering and Technology, Third Xiangya Hospital, Central South University, Changsha 410013, China.
Ying
Y
Niu
Research Center of National Health Ministry on Transplantation Medicine Engineering and Technology, Third Xiangya Hospital, Central South University, Changsha 410013, China.
Qianwen
Q
Liu
Research Center of National Health Ministry on Transplantation Medicine Engineering and Technology, Third Xiangya Hospital, Central South University, Changsha 410013;. Institute of Hepatobiliary Diseases, Zhongnan Hospital of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan 430071, China.
Qifa
Q
Ye
D017209:Apoptosis; D006801:Humans; D007093:Imidazoles; D007211:Indoles; D007249:Inflammation; D009336:Necrosis; D053422:Receptor-Interacting Protein Serine-Threonine Kinases; D015427:Reperfusion Injury
D007093:Imidazoles; D007211:Indoles; C507699:necrostatin-1; C506249:RIPK1 protein, human; D053422:Receptor-Interacting Protein Serine-Threonine Kinases