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Shared mechanisms of multimorbidity in COPD, atherosclerosis and type-2 diabetes: the neutrophil as a potential
Michael J Hughes1, Helen M McGettrick2, Elizabeth Sapey3
1Birmingham Acute Care Research Group, Institute of Inflammation and Ageing, University of Birmingham, Birmingham, UK mxh619@bham.ac.uk.
Insights
Common mechanisms link chronic obstructive pulmonary disease (COPD), type-2 diabetes mellitus (T2D), and atherosclerosis. This review explores shared pathways like inflammation and cellular aging, identifying potential therapeutic targets for multimorbidity.
Area of Science:
- * Integrative biology and pathophysiology of chronic diseases.
- * Focus on shared mechanisms in multimorbidity.
Background:
- * Multimorbidity is rising, challenging current healthcare models.
- * COPD, T2D, and atherosclerosis frequently co-occur, suggesting shared etiological factors beyond traditional risks.
- * Neutrophilic inflammation is implicated in all three conditions, potentially linking them.
Purpose of the Study:
- * To review the scientific evidence linking COPD, T2D, and atherosclerosis.
- * To explore common pathogenic mechanisms including inflammation, cellular senescence, and phenotypic changes.
- * To identify and evaluate emerging therapeutic strategies targeting these shared pathways.
Main Methods:
- * Comprehensive literature review of current scientific evidence.
- * Analysis of studies focusing on inflammation, cellular aging, and cellular processes (ROS, phenotypic changes).
- * Synthesis of findings related to the pathogenesis of COPD, T2D, and atherosclerosis.
Main Results:
- * Neutrophilic inflammation is a key shared mechanism in COPD, T2D, and atherosclerosis.
- * Cellular senescence and altered cellular phenotypes are increasingly recognized as common contributors.
- * Evidence suggests a systemic inflammatory milieu contributes to multimorbidity progression.
Conclusions:
- * Inflammation and cellular aging represent unifying pathogenic mechanisms across COPD, T2D, and atherosclerosis.
- * Targeting these shared pathways offers potential for novel therapeutic approaches in multimorbidity.
- * Further research into underlying cellular biology is needed for effective multimorbid disease management.
Abstract:
Multimorbidity is increasingly common and current healthcare strategies are not always aligned to treat this complex burden of disease. COPD, type-2 diabetes mellitus (T2D) and cardiovascular disease, especially atherosclerosis, occur more frequently together than expected, even when risk factors such as smoking, obesity, inactivity and poverty are considered. This supports the possibility of unifying mechanisms that contribute to the pathogenesis or progression of each condition.Neutrophilic inflammation is causally associated with COPD, and increasingly recognised in the pathogenesis of atherosclerosis and T2D, potentially forming an aetiological link between conditions. This link might reflect an overspill of inflammation from one affected organ into the systemic circulation, exposing all organs to an increased milieu of proinflammatory cytokines. Additionally, increasing evidence supports the involvement of other processes in chronic disease pathogenesis, such as cellular senescence or changes in cellular phenotypes.This review explores the current scientific evidence for inflammation, cellular ageing and cellular processes, such as reactive oxygen species production and phenotypic changes in the pathogenesis of COPD, T2D and atherosclerosis; highlighting common mechanisms shared across these diseases. We identify emerging therapeutic approaches that target these areas, but also where more work is still required to improve our understanding of the underlying cellular biology in a multimorbid disease setting.
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