The management of cancer patients is frequently complicated by the occurrence of a complex syndrome known as cachexia. It is mainly characterized by muscle wasting, a condition that associates with enhanced protein breakdown and with negative energy balance. While the mechanisms underlying cachexia have been only partially elucidated, understanding the pathogenesis of muscle wasting in cancer hosts is mandatory in order to design new targeted therapeutic strategies. Indeed, most of cancer patients will experience cachexia during the course of their disease, and about 25% of cancer-related deaths are due to this syndrome, rather than to the tumor itself. Recent advances. Compelling evidence suggest that an altered redox homeostasis likely contributes to cancer-induced muscle protein depletion, directly or indirectly activating the intracellular degradative pathways. In addition, oxidative stress impinges on both mitochondrial number and function; the other way round, altered mitochondria lead to enhanced redox unbalance, creating a vicious loop that eventually results in negative energy metabolism.

The redox balance: a target for interventions against muscle wasting in cancer cachexia?

Penna, Fabio;Ballarò, Riccardo;Costelli, Paola
2020-01-01

Abstract

The management of cancer patients is frequently complicated by the occurrence of a complex syndrome known as cachexia. It is mainly characterized by muscle wasting, a condition that associates with enhanced protein breakdown and with negative energy balance. While the mechanisms underlying cachexia have been only partially elucidated, understanding the pathogenesis of muscle wasting in cancer hosts is mandatory in order to design new targeted therapeutic strategies. Indeed, most of cancer patients will experience cachexia during the course of their disease, and about 25% of cancer-related deaths are due to this syndrome, rather than to the tumor itself. Recent advances. Compelling evidence suggest that an altered redox homeostasis likely contributes to cancer-induced muscle protein depletion, directly or indirectly activating the intracellular degradative pathways. In addition, oxidative stress impinges on both mitochondrial number and function; the other way round, altered mitochondria lead to enhanced redox unbalance, creating a vicious loop that eventually results in negative energy metabolism.
2020
33
8
542
558
Penna, Fabio; Ballarò, Riccardo; Costelli, Paola
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/1793623
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