Macrophage metabolic reprogramming in chronic diseases

Abstract

Chronic obstructive pulmonary disease (COPD), cardiovascular disease, and diabetes are the most common chronic diseases worldwide.COPD is a progressive and debilitating respiratory condition characterized by persistent lung airflow limitation (1). It encompasses a group of chronic lung disorders, primarily chronic bronchitis, and emphysema (2). COPD gradually worsens over time, leading to significant respiratory symptoms, reduced lung function, and impaired quality of life. It is a global health concern, affecting millions of people worldwide and imposing a substantial burden on individuals, healthcare systems, and society as a whole. Understanding the causes, symptoms, diagnosis, and management of COPD is crucial in order to improve patient outcomes and alleviate the impact of this chronic respiratory condition.Diabetes mellitus is a chronic condition characterized by high blood sugar levels resulting from insulin deficiency or resistance. It can be classified into Type 1 diabetes, caused by a lack of insulin production, and Type 2 diabetes (T2DM), caused by insulin resistance. Globally, there are approximately 415 million diagnosed cases of diabetes (of which 87-91% have T2DM in high-income countries), a number expected to rise to 642 million by 2040 (3). Diabetes is a significant cause of morbidity and mortality, with complications including diabetic nephropathy, peripheral neuropathy, and cardiovascular diseases. Despite advancements in treatment and decreasing complication rates (4), the prevalence of newly diagnosed cases continues to rise (5). INFLAMMATIONCOPD is characterized by chronic inflammation that affects various tissues involved in respiratory function, including the lungs and airways. This persistent inflammation is marked by increased levels of pro-inflammatory cytokines and other immune mediators. In COPD, chronic inflammation is primarily triggered by long-term exposure to irritants, such as cigarette smoke or environmental pollutants. The inflammatory response in the lungs leads to structural changes, airway remodeling, and narrowing of the air passages, resulting in airflow limitation and respiratory symptoms. Pro-inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and others, contribute to the perpetuation of the inflammatory process and tissue damage in COPD. This chronic inflammation not only worsens respiratory symptoms but also contributes to the development of comorbidities, such as cardiovascular disease. Understanding the role of chronic inflammation in COPD is crucial for the development of targeted therapies aimed 9 11 13