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IGF-1 deficiency impairs endothelial NO bioavailability through elevation of NO breakdown due to increased generation of reactive oxygen species (ROS) and downregulation of endothelial nitric oxide synthase (eNOS) [168, 169]

Fielding CA, Jones GW, McLoughlin RM et al (2014) Interleukin-6 signaling drives fibrosis in unresolved inflammation

Although there have been few studies on the abnormal pathological states of GCs, it is known from the existing studies that the abnormal condition of GCs generated by EMS does not exist alone, but interacts with one another

in Nature demonstrated another mechanism of ferroptosis suppressor protein 1 (FSP1)-mediated ferroptosis resistance [1], motivating to summarize the anti-ferroptotic role of FSP1

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