Lung Injury Induces a Skeletal Muscle Atrophy Program That Is Qualitatively Different from That Induced by Starvation.

Files, DC; DeGorordo, Antonio; Kesari, Priya; Johnston, Laura; Tsushima, Kenji; Aggarwal, Nishant; Sidhaye, VK; D'Alessio, FR; Ls, King; Crow, MT

doi:10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6125

D97. Mediators of Skeletal Muscle Injury and Repair 2009

DOI: 10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6125

|View full text |Cite

Lung Injury Induces a Skeletal Muscle Atrophy Program That Is Qualitatively Different from That Induced by Starvation.

DC Files

Antonio DeGorordo²,

Priya Kesari³

et al.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Citation Types

Supporting

Mentioning

Contrasting

Year Published

2012

Publication Types

Select...

Article1

Relationship

Self Cite0

Independent1

Authors

Journals

Cited by 1 publication

(1 citation statement)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We tested the hypothesis that MuRF1 is necessary for the ALI-associated decrease in muscle mass and loss of contractile proteins during the period of active lung injury. Some of the results of these studies have been previously reported in abstract form (17)(18)(19).…”

mentioning

confidence: 94%

A Critical Role for Muscle Ring Finger-1 in Acute Lung Injury–associated Skeletal Muscle Wasting

Files

D’Alessio²,

Johnston³

et al. 2012

Am J Respir Crit Care Med

View full text Add to dashboard Cite

Rationale: Acute lung injury (ALI) is a debilitating condition associated with severe skeletal muscle weakness that persists in humans long after lung injury has resolved. The molecular mechanisms underlying this condition are unknown. Objectives: To identify the muscle-specific molecular mechanisms responsible for muscle wasting in a mouse model of ALI. Methods: Changes in skeletal muscle weight, fiber size, in vivo contractile performance, and expression of mRNAs and proteins encoding muscle atrophy-associated genes for muscle ring finger-1 (MuRF1) and atrogin1 were measured. Genetic inactivation of MuRF1 or electroporationmediated transduction of miRNA-based short hairpin RNAs targeting either MuRF1 or atrogin1 were used to identify their role in ALIassociated skeletal muscle wasting. Measurements and Main Results: Mice with ALI developed profound muscle atrophy and preferential loss of muscle contractile proteins associated with reduced muscle function in vivo. Although mRNA expression of the muscle-specific ubiquitin ligases, MuRF1 and atrogin1, was increased in ALI mice, only MuRF1 protein levels were up-regulated. Consistent with these changes, suppression of MuRF1 by genetic or biochemical approaches prevented muscle fiber atrophy, whereas suppression of atrogin1 expression was without effect. Despite resolution of lung injury and down-regulation of MuRF1 and atrogin1, force generation in ALI mice remained suppressed. Conclusions: These data show that MuRF1 is responsible for mediating muscle atrophy that occurs during the period of active lung injury in ALI mice and that, as in humans, skeletal muscle dysfunction persists despite resolution of lung injury.Keywords: skeletal muscle atrophy; intensive care unit-acquired weakness; critical illness myopathy; muscle atrophy genes; proteasomal-mediated protein degradation Acute lung injury (ALI) is a syndrome characterized by the acute onset of pulmonary infiltrates and respiratory failure often leading to the need for mechanical ventilation (1). Approximately 200,000 people per year develop ALI in the United States, with mortality high at 30-40% (2). A common complication associated with ALI is skeletal muscle weakness. Weakness in these patients results in decreased long-term mobility and functional status. Skeletal muscle weakness is initiated early in the course of ALI, and has been shown to persist in a large percentage of patients for up to 5 years after resolution of lung injury and hospital discharge (3-6). Although multiple factors may contribute to ALI-induced muscle atrophy including reduced nutrition, inactivity caused by bed rest, and systemic inflammation, the etiology of ALI-associated skeletal muscle atrophy remains incompletely understood.Skeletal muscle weakness is a common finding not only among patients with ALI, but also in patients with other critical illnesses. Clinically apparent weakness is present in 20-50% of patients with critical illness and has been shown to be an independent risk factor for mortality in these patients (3,5,7,8)....

show abstract

mentioning

confidence: 94%

A Critical Role for Muscle Ring Finger-1 in Acute Lung Injury–associated Skeletal Muscle Wasting

Files

D’Alessio²,

Johnston³

et al. 2012

Am J Respir Crit Care Med

View full text Add to dashboard Cite

show abstract

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

customersupport@researchsolutions.com

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Made with 💙 for researchers

Part of the Research Solutions Family.

Lung Injury Induces a Skeletal Muscle Atrophy Program That Is Qualitatively Different from That Induced by Starvation.

Cited by 1 publication

References 0 publications

A Critical Role for Muscle Ring Finger-1 in Acute Lung Injury–associated Skeletal Muscle Wasting

A Critical Role for Muscle Ring Finger-1 in Acute Lung Injury–associated Skeletal Muscle Wasting

Contact Info

Product

Resources

About