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10.1038/s41422-020-00441-1 http://scihub22266oqcxt.onion/10.1038/s41422-020-00441-1 33268902!8026611!33268902     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Res 2021 ; 31 (2): 107-125 Nephropedia Template TP {{tp|p=33268902|t=2021. Ferroptosis: molecular mechanisms and health implications |pdf=|usr=}}{{33268902}} gab.com Text Ferroptosis: molecular mechanisms and health implications JO: Cell Res http://www.kidney.de/pget.php?&tw=1&pmid=33268902 #FOAvip Cell death can be executed through different subroutines. Since the description of ferroptosis as an iron-dependent form of non-apoptotic cell death in 2012, there has been mounting interest in the process and function of ferroptosis. Ferroptosis can occur through two major pathways, the extrinsic or transporter-dependent pathway and the intrinsic or enzyme-regulated pathway. Ferroptosis is caused by a redox imbalance between the production of oxidants and antioxidants, which is driven by the abnormal expression and activity of multiple redox-active enzymes that produce or detoxify free radicals and lipid oxidation products. Accordingly, ferroptosis is precisely regulated at multiple levels, including epigenetic, transcriptional, posttranscriptional and posttranslational layers. The transcription factor NFE2L2 plays a central role in upregulating anti-ferroptotic defense, whereas selective autophagy may promote ferroptotic death. Here, we review current knowledge on the integrated molecular machinery of ferroptosis and describe how dysregulated ferroptosis is involved in cancer, neurodegeneration, tissue injury, inflammation, and infection. Twit Text FOAVip Ferroptosis: molecular mechanisms and health implications ????Cell Res http://www.kidney.de/pget.php?&tw=1&pmid=33268902 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33268902 #FOAvip English Wikipedia <ref>{{Cite pmid|33268902}}</ref> Ferroptosis: molecular mechanisms and health implications #MMPMID33268902 Tang D; Chen X; Kang R; Kroemer G Cell Res 2021[Feb]; 31 (2): 107-125 PMID33268902show ga Cell death can be executed through different subroutines. Since the description of ferroptosis as an iron-dependent form of non-apoptotic cell death in 2012, there has been mounting interest in the process and function of ferroptosis. Ferroptosis can occur through two major pathways, the extrinsic or transporter-dependent pathway and the intrinsic or enzyme-regulated pathway. Ferroptosis is caused by a redox imbalance between the production of oxidants and antioxidants, which is driven by the abnormal expression and activity of multiple redox-active enzymes that produce or detoxify free radicals and lipid oxidation products. Accordingly, ferroptosis is precisely regulated at multiple levels, including epigenetic, transcriptional, posttranscriptional and posttranslational layers. The transcription factor NFE2L2 plays a central role in upregulating anti-ferroptotic defense, whereas selective autophagy may promote ferroptotic death. Here, we review current knowledge on the integrated molecular machinery of ferroptosis and describe how dysregulated ferroptosis is involved in cancer, neurodegeneration, tissue injury, inflammation, and infection. |*Ferroptosis/genetics/immunology[MESH] |*Lipid Peroxidation[MESH] |*Signal Transduction[MESH] |Animals[MESH] |Antioxidants/*metabolism[MESH] |Autophagy[MESH] |Epigenesis, Genetic[MESH] |Humans[MESH] |Iron/*metabolism[MESH] |NF-E2-Related Factor 2[MESH] |Neoplasms/*metabolism[MESH]Ferroptosis: molecular mechanisms and health implications (epmc).pdf DeepDyve Pubget Overpricing