AMP-Activated Protein Kinase (AMPK) at the Crossroads Between CO<sub>2</sub> Retention and Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease (COPD)
Skeletal muscle dysfunction is a major comorbidity in chronic obstructive pulmonary disease (COPD) and other pulmonary conditions. Chronic CO<sub>2</sub> retention, or hypercapnia, also occur in some of these patients. Both muscle dysfunction and hypercapnia associate with higher mortali...
Main Authors: | , , |
---|---|
Format: | Article |
Language: | English |
Published: |
MDPI AG
2020-01-01
|
Series: | International Journal of Molecular Sciences |
Subjects: | |
Online Access: | https://www.mdpi.com/1422-0067/21/3/955 |
id |
doaj-97a4e736cead44ca990c30a709585e4a |
---|---|
record_format |
Article |
spelling |
doaj-97a4e736cead44ca990c30a709585e4a2020-11-25T01:45:08ZengMDPI AGInternational Journal of Molecular Sciences1422-00672020-01-0121395510.3390/ijms21030955ijms21030955AMP-Activated Protein Kinase (AMPK) at the Crossroads Between CO<sub>2</sub> Retention and Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease (COPD)Joseph Balnis0Tanner C. Korponay1Ariel Jaitovich2Division of Pulmonary and Critical Care Medicine, Albany Medical College, Albany, NY 12208, USADivision of Pulmonary and Critical Care Medicine, Albany Medical College, Albany, NY 12208, USADivision of Pulmonary and Critical Care Medicine, Albany Medical College, Albany, NY 12208, USASkeletal muscle dysfunction is a major comorbidity in chronic obstructive pulmonary disease (COPD) and other pulmonary conditions. Chronic CO<sub>2</sub> retention, or hypercapnia, also occur in some of these patients. Both muscle dysfunction and hypercapnia associate with higher mortality in these populations. Over the last years, we have established a mechanistic link between hypercapnia and skeletal muscle dysfunction, which is regulated by AMPK and causes depressed anabolism via reduced ribosomal biogenesis and accelerated catabolism via proteasomal degradation. In this review, we discuss the main findings linking AMPK with hypercapnic pulmonary disease both in the lungs and skeletal muscles, and also outline potential avenues for future research in the area based on knowledge gaps and opportunities to expand mechanistic research with translational implications.https://www.mdpi.com/1422-0067/21/3/955ampkprotein anabolismprotein catabolismcopdmuscle atrophy |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Joseph Balnis Tanner C. Korponay Ariel Jaitovich |
spellingShingle |
Joseph Balnis Tanner C. Korponay Ariel Jaitovich AMP-Activated Protein Kinase (AMPK) at the Crossroads Between CO<sub>2</sub> Retention and Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease (COPD) International Journal of Molecular Sciences ampk protein anabolism protein catabolism copd muscle atrophy |
author_facet |
Joseph Balnis Tanner C. Korponay Ariel Jaitovich |
author_sort |
Joseph Balnis |
title |
AMP-Activated Protein Kinase (AMPK) at the Crossroads Between CO<sub>2</sub> Retention and Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease (COPD) |
title_short |
AMP-Activated Protein Kinase (AMPK) at the Crossroads Between CO<sub>2</sub> Retention and Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease (COPD) |
title_full |
AMP-Activated Protein Kinase (AMPK) at the Crossroads Between CO<sub>2</sub> Retention and Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease (COPD) |
title_fullStr |
AMP-Activated Protein Kinase (AMPK) at the Crossroads Between CO<sub>2</sub> Retention and Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease (COPD) |
title_full_unstemmed |
AMP-Activated Protein Kinase (AMPK) at the Crossroads Between CO<sub>2</sub> Retention and Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease (COPD) |
title_sort |
amp-activated protein kinase (ampk) at the crossroads between co<sub>2</sub> retention and skeletal muscle dysfunction in chronic obstructive pulmonary disease (copd) |
publisher |
MDPI AG |
series |
International Journal of Molecular Sciences |
issn |
1422-0067 |
publishDate |
2020-01-01 |
description |
Skeletal muscle dysfunction is a major comorbidity in chronic obstructive pulmonary disease (COPD) and other pulmonary conditions. Chronic CO<sub>2</sub> retention, or hypercapnia, also occur in some of these patients. Both muscle dysfunction and hypercapnia associate with higher mortality in these populations. Over the last years, we have established a mechanistic link between hypercapnia and skeletal muscle dysfunction, which is regulated by AMPK and causes depressed anabolism via reduced ribosomal biogenesis and accelerated catabolism via proteasomal degradation. In this review, we discuss the main findings linking AMPK with hypercapnic pulmonary disease both in the lungs and skeletal muscles, and also outline potential avenues for future research in the area based on knowledge gaps and opportunities to expand mechanistic research with translational implications. |
topic |
ampk protein anabolism protein catabolism copd muscle atrophy |
url |
https://www.mdpi.com/1422-0067/21/3/955 |
work_keys_str_mv |
AT josephbalnis ampactivatedproteinkinaseampkatthecrossroadsbetweencosub2subretentionandskeletalmuscledysfunctioninchronicobstructivepulmonarydiseasecopd AT tannerckorponay ampactivatedproteinkinaseampkatthecrossroadsbetweencosub2subretentionandskeletalmuscledysfunctioninchronicobstructivepulmonarydiseasecopd AT arieljaitovich ampactivatedproteinkinaseampkatthecrossroadsbetweencosub2subretentionandskeletalmuscledysfunctioninchronicobstructivepulmonarydiseasecopd |
_version_ |
1725024988267806720 |