Chemerin: A Potential Regulator of Inflammation and Metabolism for Chronic Obstructive Pulmonary Disease and Pulmonary Rehabilitation

الملخص EN

Chronic obstructive pulmonary disease (COPD) features chronic inflammatory reactions of both intra- and extrapulmonary nature.

Moreover, COPD is associated with abnormal glucose and lipid metabolism in patients, which influences the prognosis and chronicity of this disease.

Abnormal glucose and lipid metabolism are also closely related to inflammation processes.

Further insights into the interactions of inflammation and glucose and lipid metabolism might therefore inspire novel therapeutic interventions to promote lung rehabilitation.

Chemerin, as a recently discovered adipokine, has been shown to play a role in inflammatory response and glucose and lipid metabolism in many diseases (including COPD).

Chemerin recruits inflammatory cells to sites of inflammation during the early stages of COPD, leading to endothelial barrier dysfunction, early vascular remodeling, and angiogenesis.

Moreover, it supports the recruitment of antigen-presenting cells that guide immune cells as part of the body’s inflammatory responses.

Chemerin also regulates metabolism via activation of its cognate receptors.

Glucose homeostasis is affected via effects on insulin secretion and sensitivity, and lipid metabolism is changed by increased transformation of preadipocytes to mature adipocytes through chemerin-binding receptors.

Controlling chemerin signaling may be a promising approach to improve various aspects of COPD-related dysfunction.

Importantly, several studies indicate that chemerin expression in vivo is influenced by exercise.

Although available evidence is still limited, therapeutic alterations of chemerin activity may be a promising target of therapeutic approaches aimed at the rehabilitation of COPD patients based on exercises.

In conclusion, chemerin plays an essential role in COPD, especially in the inflammatory responses and metabolism, and has a potential to become a target for, and a biomarker of, curative mechanisms underlying exercise-mediated lung rehabilitation.