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Cellular and Molecular Mechanisms in Gynecological Disorders

By: Contributor(s): Resource type: Ressourcentyp: Buch (Online)Book (Online)Language: English Publisher: CH : MDPI - Multidisciplinary Digital Publishing Institute, 2025Description: 1 Online-Ressource (1 electronic resource 376 p.)ISBN:
  • 9783725854134
  • 9783725854141
Subject(s): Online resources: Summary: Gynecological disorders encompass a broad spectrum of conditions affecting the female reproductive organs, including the uterus, ovaries, fallopian tubes, cervix, vagina, and external genitalia. These diseases impose a major health and financial burden worldwide, causing significant morbidity and profoundly affecting women’s quality of life. Despite their prevalence, the underlying etiologies are often complex and remain only partially understood, with limited knowledge of the risk factors that contribute to disease onset and progression. Advancing our understanding of the cellular and molecular mechanisms driving these disorders is therefore essential for developing more effective strategies for prevention, diagnosis, and treatment. This collection of original research and review articles provides a comprehensive overview of emerging insights into ovarian and uterine pathologies, reflecting the interconnected nature of gynecologic conditions. Topics addressed include mesothelial clearance by endometriosis spheroids, impaired decidualization, autophagy in reproductive aging, protease regulation in ovarian function, immune–tumor interactions in ovarian cancer, and the molecular drivers of fibrosis, senescence, cellular transformation, and tumorigenesis in uterine tissues. Collectively, these contributions underscore the urgent need for integrative research efforts that bridge basic science and clinical application, ultimately advancing the field toward improved outcomes for women affected by gynecologic diseasesPPN: PPN: 1983969532Package identifier: Produktsigel: ZDB-94-OAB
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Namensnennung 4.0 International CC BY 4.0 cc:

https://creativecommons.org/licenses/by/4.0/

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