Obesity:癌症与肥胖的因果关系

2021-06-10 Viho MedSci原创

肥胖与至少13种癌症发展或死亡的风险增加有关。据估计,11%的女性癌症和5%的男性癌症可归因于超重和肥胖。

肥胖与至少13种癌症发展或死亡的风险增加有关。据估计,11%的女性癌症和5%的男性癌症可归因于超重和肥胖。然而,肥胖刺激致癌的具体生物学机制尚不完全清楚。肿瘤的发生受多种因素的影响,这些因素来自于功能失调和肥大的内脏脂肪组织。过度肥胖会引起机体代谢、免疫和内分泌系统的改变,导致胰岛素、胰岛素样生长因子(IGF)、性激素、脂质、细胞因子和脂肪因子(包括瘦素)的异常浓度和信号传导。

尽管有证据显示,肥胖会增加癌症进展的风险,但仍需努力确定免疫抑制细胞与肥胖症患者免疫疗法反应之间的因果关系。

最近发表在Obesity杂志上的研究发现,具有免疫抑制特性的炎症细胞---骨髓源性抑制细胞(MDSCs)可能作为肥胖与癌症风险、进展和转移之间的一个关键生物联系。这些发现推进了有关肥胖相关炎症和癌症之间联系。

髓系细胞的功能是由代谢微环境决定的。在肥胖症中易产生巨噬细胞和具有免疫抑制特性的骨髓细胞---骨髓源性抑制细胞(MDSCs)。与肥胖症的代谢性炎症有关的主要因素之一是MDSCs的增加。在癌症患者中,MDSCs与生存率低和对免疫疗法的抵抗有关。

人们普遍认为,在正常体重和代谢稳态的情况下,具有抗炎作用的M2巨噬细胞是浸润脂肪组织的主要巨噬细胞亚群。一旦肥胖增加(超重),就会发生从M2M1前炎症极化巨噬细胞的转变。这个开关被认为是肥胖相关炎症的关键。

 但该研究人员发现,随着肥胖的发展和胰岛素抵抗的发展,M2巨噬细胞在脂肪组织中的增殖出现M2交替激活状态的标记物。在肥胖晚期,为了解决炎症、修复组织和恢复胰岛素敏感性,其他具有免疫调节、血管生成和组织重塑活性的髓样细胞(MdSCs)也浸润脂肪组织。虽然这些髓系细胞恢复了代谢平衡并解决了炎症,但它们的持续存在孕育了一种免疫抑制和血管生成的微环境,促进了新出现的恶性细胞的免疫逃逸和肿瘤的发生。

肥胖所致炎症在肿瘤发展演变中的作用。

虽然炎症和代谢/内分泌紊乱之间存在巨大的交叉作用,促进了肥胖症患者的肿瘤生长,但此前对于生物和分子机制并不完全了解。研究人员对相关研究进行系统分析后解释说,肥胖症中的代谢因素,如脂质、胰岛素和瘦素的改变,有助于激活骨髓细胞的免疫抑制和癌症发展能力。

该研究结果显示,MDSCs是免疫抑制和炎症的重要驱动因素,也促进肿瘤的发展。破译了肥胖相关的代谢因素激活或增强MDSCs和免疫抑制性巨噬细胞功能的分子机制。该研究结论将使医学界能够确定预后和治疗反应的生物标志物,还将发现破坏肥胖和癌症之间的病理生理学炎症联系的药理治疗的潜在目标。

文章参考:Maria Dulfary SanchezPino, Linda Anne Gilmore, Augusto C. Ochoa, Justin C. Brown. ObesityAssociated Myeloid Immunosuppressive Cells, Key Players in Cancer Risk and Response to ImmunotherapyObesity, 2021; 29 (6): 944 DOI: 10.1002/oby.23108

 

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    2021-07-27 zhanglin3079
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    2021-06-12 lingaifan
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    2021-06-11 ms5000001756152328

    学到了

    0

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    2021-06-11 ms3596413418274757

    减肥是终身任务

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    2021-06-10 1483f8cem53(暂无昵称)

    又学到一些

    0

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    2021-06-10 旭日2

    学习

    0

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