Key result
Intact aged perivascular adipose tissue increases aortic stiffness, driven by fibrotic remodeling.
Why the study?
It is unknown whether aortic perivascular adipose tissue maintains its positive influence on aortic compliance with advancing age.
Does intact aortic perivascular adipose tissue exacerbate aortic stiffness in aged mice?
Does intact aortic perivascular adipose tissue exacerbate aortic stiffness in aged mice?
Aged aortic perivascular adipose tissue undergoes fibrotic remodeling and exerts a detrimental influence on aortic stiffness in mice.
Aging is characterized by progressive large artery stiffening, a major risk factor for cardiovascular disease. The aorta is surrounded by aortic perivascular adipose tissue (APVAT), which has been shown to contribute to greater compliance in young healthy rodents in ex vivo assessments of aortic stiffness. However, whether APVAT maintains this positive influence on compliance with advancing age is unknown. Therefore, we assessed ex vivo aortic stiffness with APVAT either intact or removed in young (4–6 mo) and old (22–25 mo) mice. In young mice, aortic stiffness did not differ between vessels with intact APVAT and those with APVAT removed. In contrast, in old mice, aortic stiffness was significantly greater when APVAT was left intact compared with cleaned aortas, indicating that aged APVAT exerts a detrimental influence on aortic stiffness. To explore potential mechanisms, we assessed collagen deposition within APVAT and found that aged mice exhibited significantly greater APVAT‑specific collagen accumulation compared with young animals. These findings suggest that with aging, APVAT undergoes fibrotic remodeling that contributes to increased aortic stiffness.
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Buckley et al. (2026) studied Aortic stiffness. Intact aortic perivascular adipose tissue (APVAT) vs. Removed APVAT (cleaned aortas) was evaluated on Ex vivo aortic stiffness. In old mice, intact aortic perivascular adipose tissue significantly increased ex vivo aortic stiffness compared with cleaned aortas due to age-related fibrotic remodeling.
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