Metabolism and skeletal muscle homeostasis in lung disease

Ermelinda Ceco, Samuel E. Weinberg, Navdeep S. Chandel, Jacob I. Sznajder*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

10 Scopus citations

Abstract

There is increased awareness that patients with lung diseases develop muscle dysfunction. Muscle dysfunction is a major contributor to a decreased quality of life in patients with chronic pulmonary diseases. Furthermore, muscle dysfunction exacerbates lung disease outcome, as a decrease in muscle mass and function are associated with increased morbidity, often long after critical illness or lung disease has been resolved. As we are learning more about the role of metabolism in health and disease, we are appreciating more the direct role of metabolism in skeletal muscle homeostasis. Altered metabolism is associated with numerous skeletal muscle pathologies and, conversely, skeletal muscle diseases are associated with significant changes in metabolic pathways. In this review, we highlight the role of metabolism in the regulation of skeletal muscle homeostasis. Understanding the metabolic pathways that underlie skeletal muscle wasting is of significant clinical interest for critically ill patients as well as patients with chronic lung disease, in which proper skeletal muscle function is essential to disease outcome.

Original languageEnglish (US)
Pages (from-to)28-34
Number of pages7
JournalAmerican journal of respiratory cell and molecular biology
Volume57
Issue number1
DOIs
StatePublished - Jul 2017

Keywords

  • Acute respiratory distress syndrome
  • Chronic obstructive pulmonary disease
  • Metabolic maladaptations
  • Satellite cells
  • Skeletal muscle homeostasis

ASJC Scopus subject areas

  • Molecular Biology
  • Pulmonary and Respiratory Medicine
  • Clinical Biochemistry
  • Cell Biology

Fingerprint Dive into the research topics of 'Metabolism and skeletal muscle homeostasis in lung disease'. Together they form a unique fingerprint.

Cite this