Tumor metabolism as a factor affecting diversity in cancer cachexia.

IF 5 2区 生物学 Q2 CELL BIOLOGY
Oliver F Bathe
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Abstract

Cancer cachexia is a multifaceted metabolic syndrome characterized by muscle wasting, fat redistribution, and metabolic dysregulation, commonly associated with advanced cancer but sometimes also evident in early-stage disease. More subtle body composition changes have also been reported in association with cancer, including sarcopenia, myosteatosis, and increased fat radiodensity. Emerging evidence reveals that body composition changes including sarcopenia, myosteatosis, and increased fat radiodensity, arise from distinct biological mechanisms and significantly impact survival outcomes. Importantly, these features often occur independently, with their combined presence exacerbating poor prognoses. Tumor plays a pivotal role in driving these host changes, either by acting as a metabolic parasite or by releasing mediators that disrupt normal tissue function. This review explores the diversity of tumor metabolism. It highlights the potential for tumor-specific metabolic phenotypes to influence systemic effects, including fat redistribution and sarcopenia. Addressing this tumor-host metabolic interplay requires personalized approaches that disrupt tumor metabolism while preserving host health. Promising strategies include targeted pharmacological interventions and anticachexia agents like growth differentiation factor 15 (GDF-15) inhibitors. Nutritional modifications such as ketogenic diets and omega-3 fatty acid supplementation also merit further investigation. In addition to preserving muscle, these therapies will need to be evaluated for their capability to improve survival and quality of life. This review underscores the need for further research into tumor-driven metabolic effects on the host and the development of integrative treatment strategies to address the interconnected challenges of cancer progression and cachexia.

肿瘤代谢是影响肿瘤恶病质多样性的因素。
癌症恶病质是一种以肌肉萎缩、脂肪再分配和代谢失调为特征的多方面代谢综合征,通常与晚期癌症相关,但有时在早期疾病中也很明显。更细微的身体组成变化也被报道与癌症有关,包括肌肉减少症、肌骨化病和脂肪放射密度增加。越来越多的证据表明,身体成分的变化,包括肌肉减少症、肌骨化症和脂肪放射密度增加,是由不同的生物学机制引起的,并显著影响生存结果。重要的是,这些特征往往是独立发生的,它们的联合存在加剧了不良预后。肿瘤在驱动这些宿主变化中起着关键作用,要么作为代谢寄生虫,要么释放破坏正常组织功能的介质。本文综述了肿瘤代谢的多样性。它强调了肿瘤特异性代谢表型影响全身效应的潜力,包括脂肪再分配和肌肉减少症。解决这种肿瘤-宿主代谢相互作用需要个性化的方法,在保持宿主健康的同时破坏肿瘤代谢。有希望的策略包括靶向药物干预和抗恶病质药物,如GDF-15抑制剂。营养调整如生酮饮食和补充omega-3脂肪酸也值得进一步研究。除了保留肌肉外,这些疗法还需要评估其改善生存和生活质量的能力。这一综述强调需要进一步研究肿瘤驱动的代谢对宿主的影响,并制定综合治疗策略,以解决癌症进展和恶病质相互关联的挑战。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
9.10
自引率
1.80%
发文量
252
审稿时长
1 months
期刊介绍: The American Journal of Physiology-Cell Physiology is dedicated to innovative approaches to the study of cell and molecular physiology. Contributions that use cellular and molecular approaches to shed light on mechanisms of physiological control at higher levels of organization also appear regularly. Manuscripts dealing with the structure and function of cell membranes, contractile systems, cellular organelles, and membrane channels, transporters, and pumps are encouraged. Studies dealing with integrated regulation of cellular function, including mechanisms of signal transduction, development, gene expression, cell-to-cell interactions, and the cell physiology of pathophysiological states, are also eagerly sought. Interdisciplinary studies that apply the approaches of biochemistry, biophysics, molecular biology, morphology, and immunology to the determination of new principles in cell physiology are especially welcome.
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