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Ferroptosis in Health and Disease

Daolin Tang
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      This updated and expanded volume gives new insights on ferroptosis – an iron-dependent form of non-apoptotic cell death. The collection of chapters discusses the two major pathways through which ferroptosis can occur: the extrinsic or transporter-dependent pathway and the intrinsic or enzyme-regulated pathway.Readers will gain an understanding of the multiple levels, on which this special cell death is regulated. Hence, the contributions will take a closer look at epigenetic, transcriptional, posttranscriptional and posttranslational layers. Among the described regulators and transcription factors are GPX4, ACSL4 and NFE2L2. This edited volume collects reviews related to current knowledge on the integrated molecular machinery of ferroptosis, thereby also describing how dysregulated ferroptosis is involved in human diseases.
      Format: Hardback CONTRIBUTORS: Daolin Tang EAN: 9783031391705 COUNTRY: Switzerland PAGES: WEIGHT: 0 g HEIGHT: 235 cm
      PUBLISHED BY: Springer International Publishing AG DATE PUBLISHED: 2023-11-06 CITY: GENRE: WIDTH: 155 cm SPINE:

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      Daolin TangDr Tang’s work chiefly focuses on designing and conducting molecular, cellular, and animal studies to investigate the mechanisms of damage-associated molecular pattern molecule (DAMP) release and activity in autophagy and cell death, and to evaluate novel drug candidates for the treatment of various inflammatory diseases, including cancer. His past contributions to biomedical science include the initial description of the role of high-mobility group box 1 (HMGB1), a classical DAMP, in autophagy. His recent contributions to DAMP biology include the identification of a novel function and activity of HMGB1 in infection and sterile inflammation. More recently, he has also identified a number of regulators of necroptosis, ferroptosis, pyroptosis, and alkaliptosis. In summary, Dr Tang is an outstanding investigator with a proven track record of innovation and achievement in the fields of DAMP, autophagy, and cell death.
      This updated and expanded volume gives new insights on ferroptosis – an iron-dependent form of non-apoptotic cell death. The collection of chapters discusses the two major pathways through which ferroptosis can occur: the extrinsic or transporter-dependent pathway and the intrinsic or enzyme-regulated pathway.Readers will gain an understanding of the multiple levels, on which this special cell death is regulated. Hence, the contributions will take a closer look at epigenetic, transcriptional, posttranscriptional and posttranslational layers. Among the described regulators and transcription factors are GPX4, ACSL4 and NFE2L2. This edited volume collects reviews related to current knowledge on the integrated molecular machinery of ferroptosis, thereby also describing how dysregulated ferroptosis is involved in human diseases.
      Format: Hardback CONTRIBUTORS: Daolin Tang EAN: 9783031391705 COUNTRY: Switzerland PAGES: WEIGHT: 0 g HEIGHT: 235 cm
      PUBLISHED BY: Springer International Publishing AG DATE PUBLISHED: 2023-11-06 CITY: GENRE: WIDTH: 155 cm SPINE:

      Book Themes:

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      Daolin TangDr Tang’s work chiefly focuses on designing and conducting molecular, cellular, and animal studies to investigate the mechanisms of damage-associated molecular pattern molecule (DAMP) release and activity in autophagy and cell death, and to evaluate novel drug candidates for the treatment of various inflammatory diseases, including cancer. His past contributions to biomedical science include the initial description of the role of high-mobility group box 1 (HMGB1), a classical DAMP, in autophagy. His recent contributions to DAMP biology include the identification of a novel function and activity of HMGB1 in infection and sterile inflammation. More recently, he has also identified a number of regulators of necroptosis, ferroptosis, pyroptosis, and alkaliptosis. In summary, Dr Tang is an outstanding investigator with a proven track record of innovation and achievement in the fields of DAMP, autophagy, and cell death.

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