Additional factors, such as increased penetration of high pressure to the thin-walled microvessels due to age-related impairment of myogenic autoregulation [69, 70], impaired IGF-1 signaling [32, 71], chronic inflammation, increased ROS production by non-mitochondrial sources, endothelial senescence, and related extracellular matrix degradation, impaired functional and structural adaptation to hypertension [69, 70, 72, 73] may contribute to microvascular fragility [6, 29, 74–76]. This evidence concerns the gene IGF1 and hypertensive disorder.