Aging-related increases in serum sex hormone-binding globulin levels in men might be related to increased synthesis

Aging in Ocular Blood Vessels: Molecular Insights and the Role of Oxidative Stress

“…However, during aging, there is a significant decline in these hormones in males, suggesting a correlation between aging, inflammation, and androgen levels [114]. One possible explanation for the age-related decline in androgens may be attributed to the increased synthesis of serum sex hormone-binding globulin, as demonstrated in a recent dedicated study [115].…”

“…Table 1 outlines the key pathophysiological drivers and their associated molecular pathways that play pivotal roles in vascular aging processes. Oxidative stress pivotal factor in vascular endothelial cell dysfunction and subsequent damage, exacerbating aging process, cell death and DNA damage in several ocular disorders [51,101] Mitochondrial dysfunction reduced mitochondrial biogenesis and SIRT activity [102,103,129] Telomere alteration telomere shortening and damage to DNA [17,103] Ca 2+ signaling anomalies remodeling processes induce impairment in Ca 2+ signals, impacting vascular function [112] Angiogenetic dysregulation, endothelial dysfunction accumulation of genetic damage and epigenetic changes affecting gene expression, leads to vascular impairment [103][104][105]133,137,138] Vascular obstruction aging may exacerbate the pro-inflammatory activity of IL-6, IL-8, and MMP-9, all agents related to retinal vascular occlusion [139][140][141][142][143] Androgen decline enhanced synthesis of the serum sex hormone-binding globulin may lead to a reduced level of androgens, which physiologically exert an anti-inflammatory effect [114,115] Traffic noise and air pollution exposure -Traffic noise exposure: alteration in stress hormone levels and heart rate as well as establishment of neuroinflammation. -Air pollution: ultrafine particles induce immune reactions and ROS formation.collectively, these factors trigger mitochondrial dysfunction, oxidative stress, telomere shortening, and chronic inflammation [116,117] UV exposure raised ROS formation, and subsequently elevated VEGF, MMP-2, and MMP-9, causing neoangiogenesis and degradation of ECM [122] High myopia age-related decreased tissue perfusion and loss of endothelial cells, aggravating the reduced ocular blood flow in high myopia [68,82,126,127]…”