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Updated: Sep 20, 2025

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Multidisciplinary Approach to Obesity Management: A Case Report
Published on: May 30, 2025
367
肥胖与恶性瘤的联系背后的机制:一个系统的叙事审查
1Molecular Biology and Human Genetics Laboratory, Dr. Panjwani Center for Molecular Medicine and Drug Research (PCMD), International Center for Chemical and Biological Sciences (ICCBS), University of Karachi, Karachi, 75270, Pakistan.
Journal of physiology and biochemistry
|May 23, 2025
概括
肥胖会通过荷尔蒙失衡,炎症和新的分子通路显著增加癌症风险. 这些影响即使在减肥后也可能持续存在,这凸显了综合预防策略的必要性.
科学领域:
- 在瘤学瘤学.
- 代谢综合征是代谢综合征的一种.
- 分子生物学分子生物学
背景情况:
- 肥胖是一个主要的公共卫生问题,与癌症发病率和进展的增加有关.
- 许多细胞和分子机制调解肥胖和癌症之间的关系.
- 了解这些机制对于制定有效的癌症预防和治疗策略至关重要.
研究的目的:
- 系统地审查和综合当前关于肥胖与癌症风险和进展有关的机制的研究.
- 为了确定新的分子途径和表观遗传修饰涉及到肥胖驱动的瘤发生.
- 突出未来研究领域和潜在的治疗目标.
主要方法:
- 系统叙事审查遵循系统审查和元分析 (PRISMA) 准则的首选报告项目.
- 在多个数据库中进行了全面的文献搜索,从1,288个初始出版物中获得了221篇精选文章.
- 对涉及肥胖相关癌症的细胞,分子,激素和表观遗传机制的分析.
主要成果:
- 肥胖通过荷尔蒙失衡 (如雌激素,胰岛素抵抗) 和慢性炎症促进癌症.
- 新的机制包括脂肪组织的分泌物,细胞外囊泡的转移,代谢重编程 (CD36,FABP4,CPT1A) 和耐铁灭.
- 表观遗传记忆 (基因组和DNA甲基化,通过FTO修改RNA) 维持体重减轻后的癌症风险.
- 器官/细胞大小的扩大增加了突变的易感性;VHL-HIF,PRDM16/UCP1,STAT3/FABP4和YAP/TAZ通路都参与其中.
结论:
- 肥胖通过多样化和复杂的分子和细胞途径显著提高癌症风险.
- 脂肪组织中的表观遗传改变和代谢重编程是导致肥胖致癌的关键驱动因素.
- 未来的研究应该专注于减肥药物,不同的人口统计,生物标志物,并整合用于新型治疗目标和预防策略的先进方法.
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