Aging is accompanied by complex alterations in immune function, characterized by immunosenescence and a chronic, low-grade inflammatory state known as inflammaging. Both phenomena play critical roles in the triggering and progression of cardiovascular diseases, including atherosclerosis, heart failure, and vascular dysfunction. Immunosenescence involves the remodeling of immune organs, declines in immune cell diversity, function, and surveillance, leading to impaired resolution of inflammation and increased susceptibility to infection and tissue damage. Concurrently, inflammaging manifests through the persistent activation of inflammatory pathways, increased levels of pro-inflammatory cytokines (e.g., IL-1β, IL-6, TNF-α), oxidative stress, and the accumulation of senescent cells, including immune cells, with a pro-inflammatory secretory phenotype. The interplay between immunosenescence and inflammaging creates a self-amplifying cycle that exacerbates endothelial dysfunction, promotes the formation and instability of atherosclerotic plaques, and impairs cardiovascular repair mechanisms.
This Research Topic aims to elucidate molecular and cellular mechanisms underlying immunosenescence and inflammaging in the cardiovascular system, their contributions to disease onset and progression, and their implications for emerging therapeutic strategies.
We welcome original research and comprehensive reviews that address the biology of immune aging, immune-endothelial interactions, mitochondrial dysfunction, inflammasome activation, the senescence-associated secretory phenotype (SASP), sex differences, and novel interventions targeting these pathways to improve cardiovascular health in the aging population.
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This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:
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