2026-04-14T02:22:46Zhttps://recercat.cat/oai/request

oai:recercat.cat:2445/1533072025-12-04T21:10:31Zcom_2072_1057col_2072_478781col_2072_478917

00925njm 22002777a 4500 dc Penna, Fabio author Ballaro, Riccardo author Martínez Cristóbal, Paula author Sala Cano, David author Sebastián Muñoz, David author Busquets Rius, Sílvia author Muscaritoli, Maurizio author Argilés Huguet, Josep Ma. author Costelli, Paola author Zorzano Olarte, Antonio author 2020-03-23T10:53:41Z 2020-07-12T05:10:23Z 2019-07-12 2020-03-23T10:53:42Z Cancer cachexia is a multifactorial syndrome characterized by anorexia, weight loss and muscle wasting that impairs patients' quality of life and survival. Aim of this work was to evaluate the impact of either autophagy inhibition (knocking down beclin-1) or promotion (overexpressing TP53INP2/DOR) on cancer-induced muscle wasting. In C26 tumor-bearing mice, stress-induced autophagy inhibition was unable to rescue the loss of muscle mass and worsened muscle morphology. Treating C26-bearing mice with formoterol, a selective β2-agonist, muscle sparing was paralleled by reduced static autophagy markers, although the flux was maintained. Conversely, the stimulation of muscle autophagy exacerbated muscle atrophy in tumor-bearing mice. TP53INP2 further promoted atrogene expression and suppressed mitochondrial dynamics-related genes. Excessive autophagy might impair mitochondrial function through mitophagy. Consistently, tumor-induced mitochondrial dysfunction was detected by reduced ex vivo muscle fiber respiration. Overall, the results evoke a central role for muscle autophagy in cancer-induced muscle wasting. Autofàgia Caquèxia Autophagy Cachexia Autophagy exacerbates muscle wasting in cancer cachexia and impairs mitochondrial function