Involvement of Parkin-mediated mitophagy in the pathogenesis of chronic obstructive pulmonary disease-related sarcopenia.


Journal

Journal of cachexia, sarcopenia and muscle
ISSN: 2190-6009
Titre abrégé: J Cachexia Sarcopenia Muscle
Pays: Germany
ID NLM: 101552883

Informations de publication

Date de publication:
06 2022
Historique:
revised: 19 02 2022
received: 03 09 2021
accepted: 28 02 2022
pubmed: 5 4 2022
medline: 11 6 2022
entrez: 4 4 2022
Statut: ppublish

Résumé

Sarcopenia is characterized by the loss of skeletal muscle mass and strength and is associated with poor prognosis in patients with chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) exposure, a major cause for COPD, induces mitochondrial damage, which has been implicated in sarcopenia pathogenesis. The current study sought to examine the involvement of insufficient Parkin-mediated mitophagy, a mitochondrion-selective autophagy, in the mechanisms by which dysfunctional mitochondria accumulate with excessive reactive oxygen species (ROS) production in the development of COPD-related sarcopenia. The involvement of Parkin-mediated mitophagy was examined using in vitro models of myotube formation, in vivo CS-exposure model using Parkin Cigarette smoke extract (CSE) induced myotube atrophy with concomitant 30% reduction in Parkin expression levels (P < 0.05). Parkin-mediated mitophagy regulated myotube atrophy by modulating mitochondrial damage and mitochondrial ROS production. Increased mitochondrial ROS was responsible for myotube atrophy by activating Muscle Ring Finger 1 (MuRF-1)-mediated myosin heavy chain (MHC) degradation. Parkin Taken together, COPD-related sarcopenia can be attributed to insufficient Parkin-mediated mitophagy and increased mitochondrial ROS causing enhanced muscle atrophy through MuRF-1 activation, which may be at least partly preventable through optimal physical exercise.

Sections du résumé

BACKGROUND
Sarcopenia is characterized by the loss of skeletal muscle mass and strength and is associated with poor prognosis in patients with chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) exposure, a major cause for COPD, induces mitochondrial damage, which has been implicated in sarcopenia pathogenesis. The current study sought to examine the involvement of insufficient Parkin-mediated mitophagy, a mitochondrion-selective autophagy, in the mechanisms by which dysfunctional mitochondria accumulate with excessive reactive oxygen species (ROS) production in the development of COPD-related sarcopenia.
METHODS
The involvement of Parkin-mediated mitophagy was examined using in vitro models of myotube formation, in vivo CS-exposure model using Parkin
RESULTS
Cigarette smoke extract (CSE) induced myotube atrophy with concomitant 30% reduction in Parkin expression levels (P < 0.05). Parkin-mediated mitophagy regulated myotube atrophy by modulating mitochondrial damage and mitochondrial ROS production. Increased mitochondrial ROS was responsible for myotube atrophy by activating Muscle Ring Finger 1 (MuRF-1)-mediated myosin heavy chain (MHC) degradation. Parkin
CONCLUSIONS
Taken together, COPD-related sarcopenia can be attributed to insufficient Parkin-mediated mitophagy and increased mitochondrial ROS causing enhanced muscle atrophy through MuRF-1 activation, which may be at least partly preventable through optimal physical exercise.

Identifiants

pubmed: 35373498
doi: 10.1002/jcsm.12988
pmc: PMC9178376
doi:

Substances chimiques

Reactive Oxygen Species 0
Ubiquitin-Protein Ligases EC 2.3.2.27
parkin protein EC 2.3.2.27

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1864-1882

Subventions

Organisme : JSPS KAKENHI Grant
Organisme : GSK Japan Research Grant 2018

Informations de copyright

© 2022 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders.

Références

Am J Physiol Lung Cell Mol Physiol. 2001 Aug;281(2):L403-11
pubmed: 11435215
Autophagy. 2015;11(3):547-59
pubmed: 25714760
COPD. 2013 Oct;10(5):618-24
pubmed: 23844868
Autophagy. 2019 Mar;15(3):510-526
pubmed: 30290714
Int J Mol Sci. 2020 Oct 28;21(21):
pubmed: 33126429
Nat Cell Biol. 2010 Feb;12(2):119-31
pubmed: 20098416
Hum Mol Genet. 2008 Dec 15;17(24):3897-908
pubmed: 18782848
Autophagy. 2017 Aug 3;13(8):1420-1434
pubmed: 28613983
J Vis Exp. 2014 Mar 27;(85):
pubmed: 24747372
J Clin Invest. 2007 Nov;117(11):3551-62
pubmed: 17965775
Am J Physiol Lung Cell Mol Physiol. 2009 Jul;297(1):L109-14
pubmed: 19411310
J Physiol. 2019 Apr;597(7):1975-1991
pubmed: 30614532
J Cachexia Sarcopenia Muscle. 2022 Jun;13(3):1864-1882
pubmed: 35373498
Am J Respir Cell Mol Biol. 2010 Apr;42(4):461-71
pubmed: 19520920
Am J Respir Crit Care Med. 2018 Jul 15;198(2):175-186
pubmed: 29554438
Muscle Nerve. 2002 Mar;25(3):383-9
pubmed: 11870715
Am J Respir Crit Care Med. 2002 Sep 15;166(6):809-13
pubmed: 12231489
J Am Med Dir Assoc. 2020 Mar;21(3):300-307.e2
pubmed: 32033882
Cell Metab. 2009 Dec;10(6):507-15
pubmed: 19945408
Thorax. 2007 Feb;62(2):115-20
pubmed: 17090575
Cell. 2011 Sep 2;146(5):682-95
pubmed: 21884931
Eur Respir J. 2009 May;33(5):1165-85
pubmed: 19407051
J Cachexia Sarcopenia Muscle. 2021 Dec;12(6):2259-2261
pubmed: 34904399
Eur Respir Rev. 2015 Jun;24(136):159-72
pubmed: 26028628
BMC Pulm Med. 2020 Mar 23;20(1):74
pubmed: 32293377
Adv Exp Med Biol. 2013;788:7-17
pubmed: 23835952
Eur Respir J. 2019 May 18;53(5):
pubmed: 30846476
Am J Respir Crit Care Med. 2013 Dec 1;188(11):1313-20
pubmed: 24228729
Free Radic Biol Med. 2016 Sep;98:218-230
pubmed: 26738803
Am J Respir Crit Care Med. 2015 Mar 15;191(6):620-5
pubmed: 25581779
J Neurol Sci. 1973 Jan;18(1):111-29
pubmed: 4120482
Am J Physiol Cell Physiol. 2013 Mar 1;304(5):C422-30
pubmed: 23220115
Sci Rep. 2018 Oct 9;8(1):15007
pubmed: 30302028
FASEB J. 2014 Apr;28(4):1621-33
pubmed: 24371120
PLoS One. 2012;7(12):e52592
pubmed: 23300713
Cell Metab. 2007 Nov;6(5):376-85
pubmed: 17983583
Eur Respir J. 2012 Nov;40(5):1115-22
pubmed: 22362854
Thorax. 2015 Mar;70(3):213-8
pubmed: 25561517
Nat Rev Drug Discov. 2015 Jan;14(1):58-74
pubmed: 25549588
Am J Physiol Cell Physiol. 2018 Aug 1;315(2):C164-C185
pubmed: 29561660
EMBO J. 2000 Nov 1;19(21):5720-8
pubmed: 11060023
Eur Respir Rev. 2019 Nov 13;28(154):
pubmed: 31722892
Am J Physiol Endocrinol Metab. 2018 Sep 1;315(3):E404-E415
pubmed: 29812989
Am J Respir Crit Care Med. 2007 Aug 1;176(3):261-9
pubmed: 17478621
J Appl Physiol (1985). 2013 May;114(9):1273-81
pubmed: 23085958

Auteurs

Akihiko Ito (A)

Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University, Tokyo, Japan.

Mitsuo Hashimoto (M)

Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University, Tokyo, Japan.

Jun Tanihata (J)

Department of Cell Physiology, The Jikei University, Tokyo, Japan.

Sachi Matsubayashi (S)

Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University, Tokyo, Japan.

Ryoko Sasaki (R)

Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University, Tokyo, Japan.

Shota Fujimoto (S)

Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University, Tokyo, Japan.

Hironori Kawamoto (H)

Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University, Tokyo, Japan.

Yusuke Hosaka (Y)

Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University, Tokyo, Japan.

Akihiro Ichikawa (A)

Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University, Tokyo, Japan.

Tsukasa Kadota (T)

Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University, Tokyo, Japan.

Yu Fujita (Y)

Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University, Tokyo, Japan.

Daisuke Takekoshi (D)

Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University, Tokyo, Japan.

Sabro Ito (S)

Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University, Tokyo, Japan.

Shunsuke Minagawa (S)

Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University, Tokyo, Japan.

Takanori Numata (T)

Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University, Tokyo, Japan.

Hiromichi Hara (H)

Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University, Tokyo, Japan.

Tatsuki Matsuoka (T)

Department of Orthopedic Surgery, The Jikei University, Tokyo, Japan.

Jun Udaka (J)

Department of Orthopedic Surgery, The Jikei University, Tokyo, Japan.

Jun Araya (J)

Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University, Tokyo, Japan.

Mitsuru Saito (M)

Department of Orthopedic Surgery, The Jikei University, Tokyo, Japan.

Kazuyoshi Kuwano (K)

Division of Respiratory Diseases, Department of Internal Medicine, The Jikei University, Tokyo, Japan.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH