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Advances in cancer cachexia: Intersection between affected organs, mediators, and pharmacological interventions.
Biochimica et Biophysica Acta (BBA) - Reviews on Cancer ( IF 9.7 ) Pub Date : 2020-03-25 , DOI: 10.1016/j.bbcan.2020.188359
Jawed A Siddiqui 1 , Ramesh Pothuraju 1 , Maneesh Jain 2 , Surinder K Batra 3 , Mohd W Nasser 2
Affiliation  

Advanced cancer patients exhibit cachexia, a condition characterized by a significant reduction in the body weight predominantly from loss of skeletal muscle and adipose tissue. Cachexia is one of the major causes of morbidity and mortality in cancer patients. Decreased food intake and multi-organ energy imbalance in cancer patients worsen the cachexia syndrome. Cachectic cancer patients have a low tolerance for chemo- and radiation therapies and also have a reduced quality of life. The presence of tumors and the current treatment options for cancer further exacerbate the cachexia condition, which remains an unmet medical need. The onset of cachexia involves crosstalk between different organs leading to muscle wasting. Recent advancements in understanding the molecular mechanisms of skeletal muscle atrophy/hypertrophy and adipose tissue wasting/browning provide a platform for the development of new targeted therapies. Therefore, a better understanding of this multifactorial disorder will help to improve the quality of life of cachectic patients. In this review, we summarize the metabolic mediators of cachexia, their molecular functions, affected organs especially with respect to muscle atrophy and adipose browning and then discuss advanced therapeutic approaches to cancer cachexia.

中文翻译:

癌症恶病质的进展:受影响器官,介质和药物干预措施之间的交叉点。

晚期癌症患者表现出恶病质,这种病的特征是体重显着降低,主要是由于骨骼肌和脂肪组织的丧失。恶病质是癌症患者发病和死亡的主要原因之一。癌症患者食物摄入减少和多器官能量失衡加剧恶病质综合征。恶病质癌症患者对化学和放射疗法的耐受性低,并且生活质量降低。肿瘤的存在和当前针对癌症的治疗选择进一步加剧了恶病质状态,这仍然是未满足的医学需求。恶病质的发作涉及不同器官之间的串扰,导致肌肉消瘦。在了解骨骼肌萎缩/肥大和脂肪组织消瘦/褐变的分子机制方面的最新进展为开发新的靶向疗法提供了平台。因此,对这种多因素疾病的更好理解将有助于改善恶病质患者的生活质量。在这篇综述中,我们总结了恶病质的代谢介质,其分子功能,受影响的器官,尤其是与肌肉萎缩和脂肪褐变有关的部分,然后讨论了癌症恶病质的先进治疗方法。
更新日期:2020-04-20
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