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肾细胞癌(renal cell carcinoma,RCC)是泌尿系统常见肿瘤之一，最常见的病理类型即肾透明细胞癌(clear cell renal cell carcinoma,ccRCC),具有特定的组织病理学和遗传特征，约占RCC总病例的70%,在数量上占主导地位^[1-2]。其他肾脏肿瘤常被单纯归类为肾非透明细胞癌(non-clear cell carcinomaof the kidney,nccRCC)进行临床研究，包括肾乳头状细胞癌、嫌色细胞癌、集合管RCC等^[3]。临床RCC多为偶然发现，通常在患者出现胁腹痛、肉眼血尿和可触及的腹部肿块后被诊断为RCC,多为晚期进展，而晚期RCC诊疗难度高，预后较差且易复发^[2,4-5]。RCC在全球男性常诊断癌症中排名第6位，女性排名第10位，分别占所有肿瘤诊断的5%和3%,且其发病率有上升趋势^[6-7]。我国2012年RCC发病率粗略值为4.9%,且死亡率多年来居高位并呈现增长趋势^[7]。针对RCC的研究为目前临床肾脏病方面的热点，其中，脂代谢活动异常是RCC细胞最大的代谢表现之一。阐明肾癌脂代谢过程，将为寻找肾癌治疗新靶点，开发相应的药物及临床诊疗提供依据。

1 RCC的病理分类

1.1 ccRCC的特点

1.2 nccRCC特点

2 脂代谢重编程在RCC中的表现

2.1 脂质合成与摄取

2.1.1 内源性脂质合成增加

2.1.2 外源性脂质摄取增加

2.2 脂质分解代谢降低

2.3 脂质运输

2.4 脂质氧化

3 肾肿瘤脂代谢关键因子

3.1 HIF介导的脂代谢异常

3.2 SREBP及其他胆固醇相关因子

3.3 AUP1

3.4 SR-B1

4 脂质代谢产物与RCC组织微环境

4.1 TME细胞与RCC的相关性  

4.1.1 癌症相关脂肪细胞

4.1.2 癌症相关血管内皮细胞

4.1.3 癌症相关成纤维细胞间充质

4.1.4 癌症相关免疫细胞

5 讨论

本文重点讨论RCC的脂代谢变化。在肾损伤期间，肾上皮细胞重新编程其代谢途径以增加脂质积累，了解这种情况背后的机制可以为研究者提供有关RCC进展变化新的见解。目前肾癌和脂肪代谢的相关性已得到普遍证实，和脂肪代谢有关的HIF、SREBP1、FASN、ACLY、CPT1A、SCD1、FRG等都是RCC潜在治疗点，还有许多潜在的脂肪代谢标志物与肾癌的预防、发生、治疗和预后有关。目前几种具有新作用机制且具有发展前景的新药正处于临床试验的不同阶段。对于免疫治疗，抗CTLA-4抗体ipilimumab与nivolumab联合在Checkmate 016试验中显示出约40%的显著应答率^[103]。此外，基于自体树突状细胞的免疫疗法与舒尼替尼联合使用的疗效已经得到检验，并显示出早期的前景^[104]。在靶向治疗领域，目前已经开发出专门针对HIF-2的抑制剂，靶向放疗多以增强抗肿瘤免疫反应以及选择性减瘤性肾切除术，用于最初无法手术但后来在全身治疗后肿瘤明显缩小的患者^[105]。希望这方面研究的缺乏将会刺激更多更深入的研究，以获得新的分子靶点和有效的生物活性化合物，来改善肾癌患者的治疗和预后。

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