Metabolite Profiles in Inflammatory Diseases

Dear Colleagues,

Cachexia, the disease-related loss of cellular mass, is a sign of the close connection between inflammation and metabolic processes. It was given the name "cachexin" because it was discovered that tumor necrosis factor-alpha (TNFα) was involved in this process. The capacity of inflammatory cytokines to have such significant impacts on cellular and metabolic systems remains instructive, even if TNFα is now more widely recognized as a modulator of inflammatory responses. Chronic inflammation leads to rheumatic cachexia, and systemic inflammation, such as that observed in RA, alters metabolism. Loss of muscle mass and maintenance of fat mass are characteristics of this. Cachexia is traditionally characterized by a low body mass index. Although RA frequently causes muscle atrophy, low BMI is rare because fat mass is maintained or even increased. Rheumatoid cachexia, which affects 10–20% of RA patients with managed illness and 38% of people with active RA, is more common than the traditional low BMI cachexia, which affects 1–13% of RA patients.

It is believed that proinflammatory cytokines, including TNFα, IL1, and IL6, are the cause of the muscle loss that happens in rheumatoid cachexia. Through the ubiquitin-proteasome pathway, TNF stimulates proteolysis. Additionally, there is some evidence that cytokines may inhibit anabolic resistance, which is the increase in muscle protein synthesis that occurs in response to feeding. The degree of muscular atrophy in rheumatoid cachexia is correlated with the disease activity of RA.

This special issue provides an opportunity for researchers to share  cutting-edge findings. We welcome high-quality original research and reviews.

Dr. Rodica Pădureanu
Dr. Ionut Donoiu
Guest Editors

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