Mechanisms of ferroptosis and targeted therapeutic approaches in urological malignancies
The prevalence of urological malignancies remains a significant global health concern, particularly given the challenging prognosis for patients in advanced disease stages. Consequently, there is a pressing need to explore the molecular mechanisms that regulate the development of urological malignan...
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Published in | Cell death discovery Vol. 10; no. 1; pp. 432 - 16 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
09.10.2024
Springer Nature B.V Nature Publishing Group |
Subjects | |
Online Access | Get full text |
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Summary: | The prevalence of urological malignancies remains a significant global health concern, particularly given the challenging prognosis for patients in advanced disease stages. Consequently, there is a pressing need to explore the molecular mechanisms that regulate the development of urological malignancies to discover novel breakthroughs in diagnosis and treatment. Ferroptosis, characterized by iron-ion-dependent lipid peroxidation, is a form of programmed cell death (PCD) distinct from apoptosis, autophagy, and necrosis. Notably, lipid, iron, and glutathione metabolism intricately regulate intracellular ferroptosis, playing essential roles in the progression of various neoplasms and drug resistance. In recent years, ferroptosis has been found to be closely related to urological malignancies. This paper provides an overview of the involvement of ferroptosis in the pathogenesis and progression of urological malignancies, elucidates the molecular mechanisms governing its regulation, and synthesizes recent breakthroughs in diagnosing and treating these malignancies. We aim to provide a new direction for the clinical treatment of urological malignancies. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 |
ISSN: | 2058-7716 2058-7716 |
DOI: | 10.1038/s41420-024-02195-w |