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10.1126/sciadv.abl8920 http://scihub22266oqcxt.onion/10.1126/sciadv.abl8920 35108055!8809683!35108055     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Adv 2022 ; 8 (5): eabl8920 Nephropedia Template TP {{tp|p=35108055|t=2022. Dexamethasone sensitizes to ferroptosis by glucocorticoid receptor-induced dipeptidase-1 expression and glutathione depletion |pdf=|usr=}}{{35108055}} gab.com Text Dexamethasone sensitizes to ferroptosis by glucocorticoid receptor-induced dipeptidase-1 expression and glutathione depletion JO: Sci Adv http://www.kidney.de/pget.php?&tw=1&pmid=35108055 #FOAvip Dexamethasone is widely used as an immunosuppressive therapy and recently as COVID-19 treatment. Here, we demonstrate that dexamethasone sensitizes to ferroptosis, a form of iron-catalyzed necrosis, previously suggested to contribute to diseases such as acute kidney injury, myocardial infarction, and stroke, all of which are triggered by glutathione (GSH) depletion. GSH levels were significantly decreased by dexamethasone. Mechanistically, we identified that dexamethasone up-regulated the GSH metabolism regulating protein dipeptidase-1 (DPEP1) in a glucocorticoid receptor (GR)-dependent manner. DPEP1 knockdown reversed the phenotype of dexamethasone-induced ferroptosis sensitization. Ferroptosis inhibitors, the DPEP1 inhibitor cilastatin, or genetic DPEP1 inactivation reversed the dexamethasone-induced increase in tubular necrosis in freshly isolated renal tubules. Our data indicate that dexamethasone sensitizes to ferroptosis by a GR-mediated increase in DPEP1 expression and GSH depletion. Together, we identified a previously unknown mechanism of glucocorticoid-mediated sensitization to ferroptosis bearing clinical and therapeutic implications. Twit Text FOAVip Dexamethasone sensitizes to ferroptosis by glucocorticoid receptor-induced dipeptidase-1 expression and glutathione depletion ????Sci Adv http://www.kidney.de/pget.php?&tw=1&pmid=35108055 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35108055 #FOAvip English Wikipedia <ref>{{Cite pmid|35108055}}</ref> Dexamethasone sensitizes to ferroptosis by glucocorticoid receptor-induced dipeptidase-1 expression and glutathione depletion #MMPMID35108055 von Massenhausen A; Zamora Gonzalez N; Maremonti F; Belavgeni A; Tonnus W; Meyer C; Beer K; Hannani MT; Lau A; Peitzsch M; Hoppenz P; Locke S; Chavakis T; Kramann R; Muruve DA; Hugo C; Bornstein SR; Linkermann A Sci Adv 2022[Feb]; 8 (5): eabl8920 PMID35108055show ga Dexamethasone is widely used as an immunosuppressive therapy and recently as COVID-19 treatment. Here, we demonstrate that dexamethasone sensitizes to ferroptosis, a form of iron-catalyzed necrosis, previously suggested to contribute to diseases such as acute kidney injury, myocardial infarction, and stroke, all of which are triggered by glutathione (GSH) depletion. GSH levels were significantly decreased by dexamethasone. Mechanistically, we identified that dexamethasone up-regulated the GSH metabolism regulating protein dipeptidase-1 (DPEP1) in a glucocorticoid receptor (GR)-dependent manner. DPEP1 knockdown reversed the phenotype of dexamethasone-induced ferroptosis sensitization. Ferroptosis inhibitors, the DPEP1 inhibitor cilastatin, or genetic DPEP1 inactivation reversed the dexamethasone-induced increase in tubular necrosis in freshly isolated renal tubules. Our data indicate that dexamethasone sensitizes to ferroptosis by a GR-mediated increase in DPEP1 expression and GSH depletion. Together, we identified a previously unknown mechanism of glucocorticoid-mediated sensitization to ferroptosis bearing clinical and therapeutic implications. |Carbolines/adverse effects/pharmacology[MESH] |Cell Line[MESH] |Dexamethasone/*pharmacology[MESH] |Dipeptidases/*genetics/metabolism[MESH] |Ferroptosis/*drug effects/*genetics[MESH] |Fluorescent Antibody Technique[MESH] |GPI-Linked Proteins/genetics/metabolism[MESH] |Gene Expression Regulation/*drug effects[MESH] |Gene Knockdown Techniques[MESH] |Glutathione/*metabolism[MESH] |Humans[MESH] |Immunophenotyping[MESH] |Oxidation-Reduction/drug effects[MESH] |Piperazines/adverse effects/pharmacology[MESH]Dexamethasone sensitizes to ferroptosis by glucocorticoid receptor-ind(epmc).pdf DeepDyve Pubget Overpricing