Involvement of Skeletal Muscle Fibrocytes in sarcOpenia in Patients With Chronic ObstRuctive Pulmonary Disease
Abstract
Chronic obstructive pulmonary disease (COPD) is presently the third leading cause of death worldwide and is characterized by irreversible airflow limitation diagnosed by spirometry. COPD is currently considered as a systemic disease with predominantly respiratory involvement, associated with numerous comorbidities. Among these, muscle wasting, present in about one third of patients, is associated with a higher mortality (up to 10-fold, irrespective of the severity of the obstruction). Muscle wasting is classically characterized by a decrease in muscle strength and volume (sarcopenia), which can be defined by a decrease in the muscle mass measured by dual X-ray absorptiometry: Appendicular Skeletal Muscle Mass or ASM / height \< 7.0 kg/m2 in men and 5.5 kg/m2 in women. However, sarcopenia is largely underestimated in current clinical practice. Moreover, there is no specific treatment: only exercise training as part of respiratory rehabilitation has shown some efficiency. The underlying pathophysiological mechanisms are indeed poorly characterized.
Fibrocytes, cells derived from blood monocytes and able to migrate to different organs in order to play pro-fibrotic or pro-inflammatory roles, play a key role in bronchial obstruction. They are recruited in the blood of COPD patients during an acute exacerbation according to a CXCL12/CXCR4 chemotactic axis. Their role in COPD sarcopenia is currently unknown, but recent data show that they are involved in a mouse model of muscular…
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Evidence Hub reads this as a clinical trial, done in people. Its evidence level is 3 of 5 (Moderate · trial / cohort / secondary analysis). Trials without a large randomized design, cohorts and secondary analyses give moderate evidence. Reported size: 22 participants or records.
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