H
Hülya Bayır
Researcher at University of Pittsburgh
Publications - 248
Citations - 22491
Hülya Bayır is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: Traumatic brain injury & Cardiolipin. The author has an hindex of 62, co-authored 222 publications receiving 15702 citations. Previous affiliations of Hülya Bayır include Boston Children's Hospital & Pennsylvania State University.
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Journal ArticleDOI
Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease
Brent R. Stockwell,José Pedro Friedmann Angeli,Hülya Bayır,Ashley I. Bush,Marcus Conrad,Scott J. Dixon,Simone Fulda,Susan Gascon,Stavroula K. Hatzios,Valerian E. Kagan,Kay Noel,Xuejun Jiang,Andreas Linkermann,Maureen E. Murphy,Michael Overholtzer,Atsushi Oyagi,Gabriela Carolina Pagnussat,Jason Park,Qitao Ran,Craig S. Rosenfeld,Konstantin Salnikow,Daolin Tang,Daolin Tang,Frank M. Torti,Suzy V. Torti,Shinya Toyokuni,K. A. Woerpel,Donna D. Zhang +27 more
TL;DR: The mechanisms underlying ferroptosis are reviewed, connections to other areas of biology and medicine are highlighted, and tools and guidelines for studying this emerging form of regulated cell death are recommended.
Journal ArticleDOI
ACSL4 dictates ferroptosis sensitivity by shaping cellular lipid composition
Sebastian Doll,Bettina Proneth,Yulia Y. Tyurina,Elena Panzilius,Sho Kobayashi,Irina Ingold,Martin Irmler,Johannes Beckers,Michaela Aichler,Axel Walch,Holger Prokisch,Dietrich Trümbach,Gaowei Mao,Feng Qu,Hülya Bayır,Joachim Füllekrug,Christina Scheel,Wolfgang Wurst,Joel A. Schick,Valerian E. Kagan,José Pedro Friedmann Angeli,Marcus Conrad +21 more
TL;DR: Pharmacological targeting of ACSL4 with thiazolidinediones, a class of antidiabetic compound, ameliorated tissue demise in a mouse model of ferroptosis, suggesting that ACSL 4 inhibition is a viable therapeutic approach to preventing ferroPTosis-related diseases.
Journal ArticleDOI
Oxidized arachidonic and adrenic PEs navigate cells to ferroptosis
Valerian E. Kagan,Gaowei Mao,Feng Qu,José Pedro Friedmann Angeli,Sebastian Doll,Claudette M. St. Croix,Haider H. Dar,Bing Liu,Vladimir A. Tyurin,Vladimir B. Ritov,Alexandr A. Kapralov,Andrew A. Amoscato,Jianfei Jiang,Tamil S. Anthonymuthu,Dariush Mohammadyani,Qin Yang,Bettina Proneth,Judith Klein-Seetharaman,Simon C. Watkins,Ivet Bahar,Joel S. Greenberger,Rama K. Mallampalli,Brent R. Stockwell,Yulia Y. Tyurina,Marcus Conrad,Hülya Bayır +25 more
TL;DR: It is discovered that ferroptosis involves a highly organized oxygenation center, wherein oxidation in endoplasmic-reticulum-associated compartments occurs on only one class of phospholipids (phosphatidylethanolamines (PEs) and is specific toward two fatty acyls-arachidonoyl (AA) and AdA (AdA).
Journal ArticleDOI
Unexpected Increased Mortality After Implementation of a Commercially Sold Computerized Physician Order Entry System
Yong Y. Han,Joseph A. Carcillo,Shekhar T. Venkataraman,Robert S. B. Clark,R. Scott Watson,R. Scott Watson,Trung C. Nguyen,Hülya Bayır,Richard A. Orr +8 more
TL;DR: An unexpected increase in mortality coincident with CPOE implementation is observed, which suggests that when implementing C POE systems, institutions should continue to evaluate mortality effects, in addition to medication error rates, for children who are dependent on time-sensitive therapies.
Journal ArticleDOI
Cardiolipin externalization to the outer mitochondrial membrane acts as an elimination signal for mitophagy in neuronal cells
Charleen T. Chu,Jing Ji,Ruben K. Dagda,Jianfei Jiang,Yulia Y. Tyurina,Alexandr A. Kapralov,Vladimir A. Tyurin,Naveena Yanamala,Indira H. Shrivastava,Dariush Mohammadyani,Kent Z.Q. Wang,Jianhui Zhu,Judith Klein-Seetharaman,Krishnakumar Balasubramanian,Andrew A. Amoscato,Grigory G. Borisenko,Zhentai Huang,Aaron M. Gusdon,Amin Cheikhi,Erin Steer,Ruth Wang,Catherine J. Baty,Simon C. Watkins,Ivet Bahar,Hülya Bayır,Valerian E. Kagan +25 more
TL;DR: Red redistribution of cardiolipin serves as an ‘eat-me’ signal for the elimination of damaged mitochondria from neuronal cells as well as the engulfment of mitochondria by the autophagic system.