Abstract
Chronic Obstructive Pulmonary Disease (COPD) is a chronic inflammatory lung disease which may be complicated by development of co-morbidities including metabolic disorders. Metabolic disorders commonly associated with this disease contribute to lung function impairment and mortality. Systemic inflammation appears to be a major factor linking COPD to metabolic alterations. Adipose tissue seems to interfere with systemic inflammation in COPD patients by producing a large number of proteins, known as “adipokines”, involved in various processes such as metabolism, immunity and inflammation. There is evidence that adiponectin is an important modulator of inflammatory processes implicated in airway pathophysiology. Increased serum levels of adiponectin and expression of its receptors on lung tissues of COPD patients have recently highlighted the importance of the adiponectin pathway in this disease. Further, in vitro studies have demonstrated an anti-inflammatory activity for this adipokine at the level of lung epithelium. This review focuses on mechanisms by which adiponectin is implicated in linking COPD with metabolic disorders.
Highlights
There is a growing awareness that chronic obstructive pulmonary disease (COPD) is a lung disease restricted to pulmonary inflammation and airway remodeling [1]
A key role for systemic inflammation in development of both metabolic disorders and lung function impairment has been recently reported and, scientific interest has been focused on adipocyte-derived cytokines including adiponectin
The molecular mechanisms through which adiponectin mediates its effects in the lungs are not clearly defined; AdipoRs expression on lung epithelial cells of Chronic Obstructive Pulmonary Disease (COPD)
Summary
There is a growing awareness that chronic obstructive pulmonary disease (COPD) is a lung disease restricted to pulmonary inflammation and airway remodeling [1]. The authors suggest that metabolic syndrome biomarkers expressed soon after exposure to World Trade Center dust predicted FEV1 decline, and the systemic inflammation produced by metabolic syndrome impacted on progression to abnormal lung function in a longitudinally followed cohort [21]. Through these observations, a growing interest has been focused on the interaction between metabolic disorders and COPD; it remains still to be elucidated which biological pathway is mainly involved.
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