Targeting α7nAChR mitigates vascular aging and endothelial cell senescence through inhibiting oxidative stress and inflammation via α7nAChR/Nrf2/HO-1 signaling pathway.
Abstract
Vascular aging is recognized as critical factor contributing to the onset and progression of cardiovascular diseases, which represent a leading cause of morbidity and mortality worldwide. The α7 nicotinic acetylcholine receptor (α7nAChR) exhibits widespread expressed in the cardiovascular system and is intricately linked to a diverse array of pathologies, in cardiovascular, conditions. Research indicates that oxidative stress plays a crucial role in exacerbating endothelial dysfunction and promoting vascular aging. However, less is known regarding the role of α7nAChR in vascular aging. In this study, we employed a combination of cellular experiments, animal models, and molecular biological techniques, utilizing an agonist (PNU282987) and antagonists (Malondialdehyde, MLA) of α7nAChR as pharmacological tools to investigate the role of α7nAChR in aging-related pathologies. The expression of α7nAChR in vascular tissue decreases with age both in rats and humans. Activation of α7nAChR alleviated vascular aging in aged rats, as evidenced by improving endothelium-dependent vasodilatation and endothelial continuity, decreased senescence-associated β-galactosidase activity, phosphorylation of H2A.X
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Research summary
The paper claims that targeting α7nAChR can mitigate vascular aging and endothelial cell senescence by inhibiting oxidative stress and inflammation. This research is relevant as it addresses mechanisms underlying vascular aging, which is a significant contributor to age-related diseases and overall longevity.
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