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  • Book
    Andrés F. Florez, Hamed Alborzinia, editors.
    Summary: This book focuses on the emerging role of ferroptosis in human diseases. It gives a detailed perspective on how to induce or suppress ferroptosis to treat challenging conditions such as infectious diseases, including COVID-19, tuberculosis, parasitic diseases and cancer. The book serves as a practical guide by providing a valuable collection of all currently known activators or inhibitors of ferroptosis. It will enable readers to choose molecules for experimental design for in vitro and in vivo studies of ferroptosis. Furthermore, this volume highlights the aspects of iron metabolism and its connection to ferritinophagy, a ferritin selective autophagy, with profound implications in neurodegenerative diseases such as Alzheimer, Parkinson, Huntington and ALS. Lastly, it describes necroptosis, another important form of cell death, along with its connections to human disorders and potential crosstalk with ferroptosis. While covering basic concepts, the book delves into mechanisms and modulation of ferroptosis for treating a wide variety of human diseases thus offering a valuable and informative resource for both, scientists and clinical researchers.

    About the Editors
    1: Ferroptosis: Concepts and Definitions
    2: Overcoming Therapeutic Challenges for Pancreatic Ductal Adenocarcinoma with xCT Inhibitors
    2.1 Pancreatic Cancer Therapeutic Challenges
    2.2 Ferroptosis and PDAC
    2.2.1 xCT-Based Ferroptosis Inducers as Systemic Therapeutics for PDAC
    2.2.2 xCT-Based Early Detection of Metastasized PDAC
    2.3 Metabolic Status Dictates Sensitivity Toward Ferroptosis
    2.4 Promoting Ferroptosis and Antigenicity in PDAC 2.5 How Stromal Compartment Influences Sensitivity to Ferroptosis
    2.6 Concluding Remarks
    3: Iron Homeostasis and Metabolism: Two Sides of a Coin
    3.1 Iron in Physiology and Disease
    3.1.1 Iron: Origin, Chemical Properties and Evolution
    3.1.2 Insights into the Redox Chemistry of Iron
    3.1.3 Strategies for Iron Assimilation and Transport
    3.2 Concluding Remarks
    4: The Role of NCOA4-Mediated Ferritinophagy in Ferroptosis
    4.1 Introduction
    4.2 NCOA4-Mediated Ferritinophagy
    4.3 NCOA4-Mediated Ferritinophagy and Ferroptosis 4.4 Ferritinophagy and Ferroptosis in Cancer
    4.5 Ferritinophagy and Ferroptosis in Neurodegeneration
    4.5.1 Neuroferritinopathy
    4.5.2 Alzheimer's Disease
    4.5.3 Parkinson's Disease
    4.5.4 Huntington's Disease
    4.5.5 Amyotrophic Lateral Sclerosis
    4.5.6 Brain Injury
    4.6 Conclusions and Future Directions
    5: Emerging Role for Ferroptosis in Infectious Diseases
    5.1 Introduction
    5.2 Necrosis in Infectious Diseases
    5.2.1 Pyroptosis and Necroptosis in Infectious Diseases
    5.3 Ferroptosis in Infectious Diseases 5.3.1 Pathogen-Induced Ferroptotic Cell Death Bacterial Infections
    Salmonella Typhimurium Infection
    Mycobacterium tuberculosis Infection
    Pseudomonas aeruginosa Infection
    Polymicrobial Sepsis Viral Infection Parasitic Infection
    5.4 Concluding Remarks
    6: Small Molecule Regulators of Ferroptosis
    6.1 Introduction
    6.2 Activators of Ferroptosis
    6.2.1 Targeting GPX4 Activity and Lipid Production Deficiency of GPX4 Production (Scheme 6.1
    Fig. 6.2) Boost of Lipid Production (Scheme 6.1 Fig. 6.3)
    6.2.2 GSH Depletion and Nuclear Factor (Erythroid-Derived 2)-like 2 (NrF2) Inhibition System Xc- Inhibition (Scheme 6.1
    Fig. 6.4) Alteration of GSH Metabolism (Scheme 6.1
    Fig. 6.5) NrF2 Inhibition (Scheme 6.1
    Fig. 6.6)
    6.2.3 Iron and ROS Production Labile iron Pool Enrichment (Scheme 6.2
    Fig. 6.7) Inducing ROS (Scheme 6.2
    Fig. 6.9) A Small molecule Inducer of Membrane Leakage (Scheme 6.2
    Fig. 6.10)
    6.3 Inhibitors of Ferroptosis
    Digital Access Springer 2021