Key result
Endothelial cell senescence promotes early vascular aging and atherosclerosis, driven by reactive oxygen species.
Why the study?
Aging is linked with endothelial dysfunction and vascular diseases, driven by factors such as reactive oxygen species, endothelial cell reprogramming, and early vascular aging.
This review summarizes the mechanisms linking endothelial dysfunction, reactive oxygen species, and cellular senescence to vascular aging and atherosclerosis.
Aging of the organism is inextricably linked with endothelial dysfunction and the development of vascular diseases. However, age as such is only one of the factors of vascular aging. Reactive oxygen species play an important role in the mechanisms of endothelial cell (EC) senescence and death. EC senescence can be associated with endothelial reprogramming, when cells acquire an immunological phenotype or transform into myofibroblasts (endothelial-to-immune or endothelial-to-mesenchymal transition, respectively). Atherosclerosis is one of the most prevalent vascular diseases, which initiates other, more severe diseases. The developmental mechanisms of atherosclerosis are associated not only with an increased level of “bad” cholesterol but also with lipoprotein and EC desialylation. Multiple factors related to heredity, lifestyle, or incidence and intensity of infectious diseases cause damage to ECs and thus promote early vascular aging, leading to secondary vascular diseases, accelerated body aging, cognitive impairments, and the development of neurodegenerative diseases. The review highlights some of these processes, their chronological and functional relationships.
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Гончаров et al. (2024) conducted a review in Vascular diseases and aging. Endothelial cell senescence and damage, driven by reactive oxygen species and other factors, promote early vascular aging and the development of atherosclerosis and secondary vascular diseases.
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