Necroptosis and its role in infectious diseases
Necroptosis is a noncaspase-dependent and precisely regulated mechanism of cell death. Necroptosis is mainly initiated by members of the tumor necrosis factor receptor (TNFR) and Toll-like receptor (TLR) families, interferon, intracellular RNA and DNA sensors and other mediators. Subsequently, the p...
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Veröffentlicht in: | Apoptosis (London) 2020-04, Vol.25 (3-4), p.169-178 |
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description | Necroptosis is a noncaspase-dependent and precisely regulated mechanism of cell death. Necroptosis is mainly initiated by members of the tumor necrosis factor receptor (TNFR) and Toll-like receptor (TLR) families, interferon, intracellular RNA and DNA sensors and other mediators. Subsequently, the protein kinase RIPK1 (receptor-interacting protein kinase 1) and RIPK3 interact with the receptor protein, which transduces death signals and further recruits and phosphorylates MLKL (mixed lineage kinase domain-like protein). MLKL serves as the initiator of cell death and eventually induces necroptosis. It was found that necroptosis is not only involved in the physiological regulation but also in the occurrence, development and prognosis of some necrotic diseases, especially infectious diseases. Intervention in the necroptosis signaling pathway is helpful for removing pathogens, inhibiting the development of lesions, and promoting the remodeling of tissue. In-depth study of the molecular regulation mechanism of necroptosis and its relationship with the pathogenesis of infectious diseases will help to provide new ideas and directions for research of the pathological mechanisms and clinical prevention of infectious diseases. |
doi_str_mv | 10.1007/s10495-019-01589-x |
format | Article |
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genetics</subject><subject>Protein Kinases - metabolism</subject><subject>Proteins</subject><subject>Receptors</subject><subject>Review</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Signal Transduction</subject><subject>Toll-like receptors</subject><subject>Tumor necrosis factor</subject><subject>Tumor necrosis factor receptors</subject><subject>Virology</subject><subject>Viruses - pathogenicity</subject><issn>1360-8185</issn><issn>1573-675X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kV1LBCEUhiWKPrb-QBcx0E03s6lHx_Eyoi9Y6qagO3H1TBizM5vOQv373LZvIlSO6PMez_ElZJ_RMaNUHSdGhZYlZTovWevyeY1sM6mgrJS8X897qGhZs1pukZ2UHimlUIPYJFvANOO8gm1yfI0u9vOhTyEVtvNFGFIR-xaL0OXZoBtCv0iFDwltwrRLNhrbJtx7jyNyd352e3pZTm4urk5PJqWTTA-lbLwDL2zVeC-ZtZRPq6kSjAvhrHKWa2gAtLUStRaytjitqQChtPMeuYQROVrlncf-aYFpMLOQHLat7TDXYzhkmDKeux2Rw1_oY7-IXa7O8EoLpSqg-l8KNOiK0fob9WBbNLn_fojWLZ82J4oLyoSCJTX-g8rD4yy4vsMm5PMfAr4S5L9OKWJj5jHMbHwxjJqll2blpclemjcvzXMWHbxXvJjO0H9KPszLAKyAlK-6B4xfLf2T9hXQKaaF</recordid><startdate>20200401</startdate><enddate>20200401</enddate><creator>Xia, Xiaojing</creator><creator>Lei, Liancheng</creator><creator>Wang, Song</creator><creator>Hu, Jianhe</creator><creator>Zhang, Gaiping</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7RQ</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>U9A</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-7717-8411</orcidid></search><sort><creationdate>20200401</creationdate><title>Necroptosis and its role in infectious diseases</title><author>Xia, Xiaojing ; Lei, Liancheng ; Wang, Song ; Hu, Jianhe ; Zhang, Gaiping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c519t-5fdc3d4a6fdd51aa02b6b741244ca7ca293f339aa5e99458aeb8043479cdde253</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Bacteria - 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Academic</collection><jtitle>Apoptosis (London)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xia, Xiaojing</au><au>Lei, Liancheng</au><au>Wang, Song</au><au>Hu, Jianhe</au><au>Zhang, Gaiping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Necroptosis and its role in infectious diseases</atitle><jtitle>Apoptosis (London)</jtitle><stitle>Apoptosis</stitle><addtitle>Apoptosis</addtitle><date>2020-04-01</date><risdate>2020</risdate><volume>25</volume><issue>3-4</issue><spage>169</spage><epage>178</epage><pages>169-178</pages><issn>1360-8185</issn><eissn>1573-675X</eissn><abstract>Necroptosis is a noncaspase-dependent and precisely regulated mechanism of cell death. Necroptosis is mainly initiated by members of the tumor necrosis factor receptor (TNFR) and Toll-like receptor (TLR) families, interferon, intracellular RNA and DNA sensors and other mediators. Subsequently, the protein kinase RIPK1 (receptor-interacting protein kinase 1) and RIPK3 interact with the receptor protein, which transduces death signals and further recruits and phosphorylates MLKL (mixed lineage kinase domain-like protein). MLKL serves as the initiator of cell death and eventually induces necroptosis. It was found that necroptosis is not only involved in the physiological regulation but also in the occurrence, development and prognosis of some necrotic diseases, especially infectious diseases. Intervention in the necroptosis signaling pathway is helpful for removing pathogens, inhibiting the development of lesions, and promoting the remodeling of tissue. 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subjects | Animals Apoptosis Bacteria - pathogenicity Biochemistry Biological response modifiers Biomedical and Life Sciences Biomedicine Cancer Research Caspases - genetics Caspases - metabolism Cell Biology Cell Death Communicable diseases Deoxyribonucleic acid DNA Humans Infections - metabolism Infections - microbiology Infections - pathology Infections - virology Infectious diseases Interferon Kinases MAP kinase Mortality Necroptosis Oncology Pathogenesis Protein kinase Protein kinases Protein Kinases - genetics Protein Kinases - metabolism Proteins Receptors Review Ribonucleic acid RNA Signal Transduction Toll-like receptors Tumor necrosis factor Tumor necrosis factor receptors Virology Viruses - pathogenicity |
title | Necroptosis and its role in infectious diseases |
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