title: Mitochondrial plasticity in cancer-related muscle wasting: potential approaches for its management.
abstract: OBJECTIVE
  Cancer cachexia represents a critical problem in clinical oncology due to its negative impact on patients' quality of life, therapeutic tolerance and survival. This paraneoplasic condition is characterized by significant weight loss mainly from skeletal muscle wasting. Understanding the molecular mechanisms underlying cancer cachexia is urgent in order to develop and apply efficient therapeutic strategies.
  
  
  RESULTS
  Mitochondrial dysfunction is an early event in cancer-induced muscle wasting. Decreased ability for ATP synthesis, impaired mitochondrial biogenesis, increased oxidative stress, impairment of protein quality control systems, increased susceptibility to mitophagy and to apoptosis were all shown to mediate contractile dysfunction and wasting in cancer cachexia. Anti-inflammatory therapies as well as exercise training seem to counteract muscle mass loss in part by improving mitochondrial functionality.
  
  
  CONCLUSIONS
  Given its central role in muscle wasting, mitochondrial plasticity should be viewed as a key therapeutic target for the preservation of muscle mass in cancer cachexia. Few studies have addressed the mitochondrial events modulated by cancer cachexia and contradictory data were reported. Scarcer studies have focused on the mitochondrial adaptation to anticancer cachexia strategies.
authors.affiliation: aQOPNA, Department of Chemistry bInstitute for Research in Biomedicine - iBiMED, Health Sciences Program, University of Aveiro, Aveiro cCIAFEL, Faculty of Sports dDepartment of Physiology and Cardiothoracic Surgery, Faculty of Medicine, University of Porto, Porto, Portugal.
authors.forename: Rui
authors.initials: R
authors.lastname: Vitorino
authors.forename: Daniel
authors.initials: D
authors.lastname: Moreira-Gonçalves
authors.forename: Rita
authors.initials: R
authors.lastname: Ferreira
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D002100:Cachexia / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy; D019468:Disease Management; D006801:Humans; D008928:Mitochondria / Q000378:metabolism / Q000502:physiology*; D018482:Muscle, Skeletal / Q000378:metabolism / Q000502:physiology*; D009133:Muscular Atrophy / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control; D009369:Neoplasms / Q000150:complications*; D018384:Oxidative Stress; D019282:Wasting Syndrome / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control; D015431:Weight Loss
chemical_list: D000255:Adenosine Triphosphate