CHAC1 inactivation is effective to preserve muscle glutathione but is insufficient to protect against muscle wasting in cachexia

PLoS One. 2023 Apr 4;18(4):e0283806. doi: 10.1371/journal.pone.0283806. eCollection 2023.

Abstract

Muscle wasting is one of the main characteristics of cachexia associated with cancer and other chronic diseases and is often exacerbated by antineoplastic agents. Increased oxidative stress is associated with muscle wasting, along with depletion of glutathione, the most abundant endogenous antioxidant. Therefore, boosting endogenous glutathione has been proposed as a therapeutic strategy to prevent muscle wasting. Here, we tested this hypothesis by inactivating CHAC1, an intracellular glutathione degradation enzyme. We found CHAC1 expression is increased under multiple muscle wasting conditions in animal models, including fasting, cancer cachexia, and chemotherapy. The elevation of muscle Chac1 expression is associated with reduced glutathione level. CHAC1 inhibition via CRSPR/Cas9 mediated knock-in of an enzyme inactivating mutation demonstrates a novel strategy to preserve muscle glutathione levels under wasting conditions but fails to prevent muscle wasting in mice. These results suggest that preserving intracellular glutathione level alone may not be sufficient to prevent cancer or chemotherapy induced muscle wasting.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cachexia* / metabolism
  • Cachexia* / prevention & control
  • Glutathione / metabolism
  • Mice
  • Muscle, Skeletal / metabolism
  • Muscular Atrophy / pathology
  • Neoplasms* / complications
  • Neoplasms* / drug therapy
  • Neoplasms* / metabolism
  • gamma-Glutamylcyclotransferase* / metabolism

Substances

  • Glutathione
  • Chac1 protein, mouse
  • gamma-Glutamylcyclotransferase

Grants and funding

All experiments were funded by Pfizer Inc. The funder provided support in the form of salaries for all authors, but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. The specific roles of these authors are articulated in the ‘author contributions’ section