Senescent Polarization of Macrophages and Inflammatory Biomarkers in Cardiovascular Disease
1Institute of Microbiology and Immunology, Faculty of Medicine, University of Ljubljana, 1000 Ljubljana, Slovenia.
Insights
Aging increases pro-inflammatory macrophages, accelerating cardiovascular disease (CVD). This review explores macrophages in vascular aging and proposes biomarkers for chronic inflammation and senotherapeutic interventions.
Area of Science:
- Cardiovascular Science
- Immunology
- Aging Research
Background:
- Cardiovascular diseases (CVDs) involve crucial inflammatory processes.
- Age-related chronic inflammation elevates blood inflammatory mediators, causing endothelial dysfunction and atherosclerosis.
- Macrophages, particularly monocyte-derived ones, are key regulators of vascular inflammation and homeostasis.
Purpose of the Study:
- To review the role of macrophages in cardiovascular aging.
- To analyze macrophage secretory phenotypes and chronic inflammation's impact on vascular integrity.
- To propose biomarkers for cardiovascular inflammation risk prediction and senotherapeutic development.
Main Methods:
- Literature review focusing on macrophages in cardiovascular aging.
- Analysis of macrophage polarization (M1 phenotype) and cytokine release (IL-1β, IL-6, IL-18).
- Examination of oxidative stress generation and its vascular effects.
Main Results:
- Monocyte-derived macrophages increase with age, promoting vascular damage and CVD.
- Aging tissue macrophages predominantly polarize to a pro-inflammatory M1 phenotype.
- This polarization releases cytokines and generates oxidative stress, impacting vascular integrity.
Conclusions:
- Macrophages significantly contribute to cardiovascular aging and disease progression through chronic inflammation.
- Understanding macrophage phenotypes and secretory profiles is crucial for targeting vascular aging.
- Identified biomarkers may improve CVD risk prediction and guide senotherapeutic strategies.
Abstract:
Cardiovascular diseases (CVDs) are a group of disorders in which inflammatory processes play a crucial role. Age-related chronic systemic inflammation is characterized by elevated levels of inflammatory mediators in the bloodstream. It can occur even in the absence of overt infection, contributing to endothelial dysfunction, vascular stiffness, and atherosclerosis. The regulation of vascular tissue homeostasis and inflammation is primarily mediated by tissue-resident macrophages (TRMs) and monocyte-derived macrophages. The proportion of monocyte-derived macrophages increases with age, contributing to vascular damage and accelerating CVD progression. In aging tissue, monocyte-derived macrophages exposed to various microenvironmental stimuli are predominantly polarized into the pro-inflammatory M1 phenotype. This polarization, in turn, triggers the release of pro-inflammatory cytokines (IL-1β, IL-6, and IL-18) and promotes the generation of oxidative stress molecules. In this review, we examine the role of macrophages in cardiovascular aging, their secretory phenotypes, and the impact of chronic low-grade inflammation on vascular integrity. We also propose reliable biomarkers of chronic cardiovascular inflammation that may aid in risk prediction, patient stratification, and the development of senotherapeutic interventions for cardiovascular disease.
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