Airborne particulate matter (PM) is a major component of air pollution and represents a significant global public health concern. Fine and ultrafine particles derived from traffic emissions, industrial processes, biomass burning, and natural sources can penetrate deep into the respiratory tract and, in some cases, enter the systemic circulation. Increasing evidence links exposure to particulate matter, particularly PM2.5 and ultrafine particles, with systemic inflammation, a key underlying mechanism in the development of cardiovascular disease, metabolic disorders, respiratory conditions, and neurodegenerative diseases. This review examines the sources and characteristics of airborne particulate matter, the biological mechanisms that connect inhaled particles to systemic inflammatory responses, and the clinical and epidemiological evidence supporting these associations. Key pathways include oxidative stress, activation of innate immune responses, endothelial dysfunction, and dysregulation of autonomic balance. The role of vulnerable populations and long-term health consequences is discussed, along with emerging biomarkers of exposure and inflammation. Finally, the review highlights policy and public health interventions aimed at reducing exposure and mitigating inflammatory health effects. Understanding the relationship between airborne particulate matter and systemic inflammation is critical for developing effective preventive strategies and reducing the global burden of pollution-related diseases.
Keywords: Particulate matter, Systemic inflammation, Oxidative stress, Cardiovascular disease, Air pollution.
Kungu Erisa· Idosr Journal of Science and...· 0 citations
Diabetes mellitus (DM) is a chronic metabolic disorder characterized by hyperglycemia and disturbances in carbohydrate, lipid, and protein metabolism. Beyond classical metabolic derangements, diabetes induces profound immunometabolic remodeling that reshapes cellular energy utilization, immune functions, and tissue homeostasis. This remodeling plays a central role in the initiation and progression of diabetic complications, including cardiovascular disease, nephropathy, neuropathy, retinopathy, and nonalcoholic fatty liver disease (NAFLD). Immunometabolic changes involve chronic low-grade inflammation, immune cell dysregulation, increased production of reactive oxygen species (ROS), and alterations in nutrient-sensing pathways such as AMP-activated protein kinase (AMPK), mechanistic target of rapamycin (mTOR), and nuclear factor kappa B (NF-κB). These pathways intersect with metabolic signaling to drive organ-specific toxicity and accelerate disease progression. This comprehensive review synthesizes current knowledge on immunometabolic interactions in diabetes, highlights mechanisms linking metabolic dysfunction and immune responses, and discusses the impact of immunometabolic remodeling on organ damage. We also evaluate emerging biomarkers and therapeutic strategies that modulate immunometabolic pathways to prevent or attenuate diabetic complications. A deeper understanding of immunometabolic remodeling offers new avenues for precision medicine in diabetes management.
Keywords: Immunometabolism, diabetes complications, inflammation, metabolic signaling, organ toxicity.
Kungu Erisa· NEWPORT INTERNATIONAL JOURNA...· 0 citations
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