Abstract
Forkhead box O3 (FOXO3) has been proposed as a homeostasis regulator, capable of integrating multiple upstream signaling pathways that are sensitive to environmental changes and counteracting their adverse effects due to external changes, such as oxidative stress, metabolic stress and growth factor deprivation. FOXO3 polymorphisms are associated with extreme human longevity. Intriguingly, longevity-associated single nucleotide polymorphisms (SNPs) in human FOXO3 correlate with lower-than-average morbidity from cardiovascular diseases in long-lived people. Emerging evidence indicates that FOXO3 plays a critical role in vascular aging. FOXO3 inactivation is implicated in several aging-related vascular diseases. In experimental studies, FOXO3-engineered human ESC-derived vascular cells improve vascular homeostasis and delay vascular aging. The purpose of this review is to explore how FOXO3 regulates vascular aging and its crucial role in aging-related vascular diseases.
Highlights
Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in individuals aged 65 years and above [1]
Another study found that longevity-associated Forkhead box O3 (FOXO3) genetic variants prolong lifespan only in individuals with cardiometabolic disease (CMD), but not in all individuals [17]. These findings show that FOXO3 may maintain cardiovascular homeostasis, promoting longevity
It is expected that research into strategies for delaying the occurrence and development of vascular aging by targeting the FOXO3 will uncover novel perspectives for the development of new drugs
Summary
Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in individuals aged 65 years and above [1]. Vascular aging has been implicated as a driver of a number of agingrelated vascular disorders [2]. A large clinical study identified two specific age-related arterial phenotypes, endothelial dysfunction, and increased arterial stiffness as independent predictors for future diagnosis of CVD [3]. At the macro level, aging vessels exhibit luminal expansion, diffused stiffness, wall thickening, and blunted angiogenesis [4, 5]. Aging vessels undergo vascular cell senescence and loss of vascular homeostasis, resulting in inflammation, oxidative stress, and calcification of blood vessels [4]. The pace of vascular aging differs in individuals due to differences in their genetics and environment background
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