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Cachexia is a prevalent multifactorial syndrome characterized by a substantial decrease in food intake, which results from processes such as proteolysis, lipolysis, inflammatory activation, and autophagy, ultimately leading to weight loss. In cancer patients, this condition is referred to as cancer-related cachexia (CRC) and affects over 50% of this population. A comprehensive understanding of the intricate interactions between tumors and the host organism is essential for the development of effective treatments for tumor cachexia. This review aims to elucidate the role of the tumor microenvironment (TME) in the pathogenesis of tumor-associated cachexia and to summarize the current evidence supporting treatment modalities that target the TME. • TME plays a crucial role in the mechanisms underlying cancer-associated cachexia. Cachexia mechanisms associated with the TME can help develop new targeted therapies and therapeutic strategies. • GDF15-GFRAL pathway, which plays an important role in cachexia development, is also a promising therapeutic target. • Leucine and phenyl acetate in urine and blood have high predictive value in cachexia diagnosis. • The therapeutic effect of FMT represents its future therapeutic value. • Cytokines such as TNF-α and cells such as TAMs all contribute to cachexia in a variety of ways.
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Shi et al. (2025) studied this question.
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