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The Molecular Mechanisms of Necroptosis and Its Role in Inflammation
Wu Chenlu, Xie Nannan, Zhou Shen’ao, Sun Liming*
State Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences,Chinese Academy of Sciences, Shanghai 200031, China
Abstract: More and more researches have shown that necrosis can happen in a precisely programmed manner， hereafter we call it programmed necrosis or necroptosis. When cells have to die but incapable of apoptosis，necroptosis then happens instead. Necroptosis is mainly induced by ligation of TNFR (tumor necrosis factor receptor) and TLR (Toll-like receptor)， and then the death receptors will recruit RIP1 (receptor interacting protein kinase1) and RIP3 (receptor interacting protein kinase 3). Subsequently， MLKL is recruited and phosphorylated by RIP3， which leads to the execution of necroptosis. Necrotic cells release cellular contents， which serves as DAMPs (damage-associated molecular pattern molecules) and induces inflammation. This review focuses on the elaborate molecular mechanism of TNF-α induced necroptosis and its critical role in inflammation induction. In addition， we will discuss the potential role of necroptosis in clinical therapy.
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