ECs are, thus, key players in the vasculature, sensing biomechanical and biochemical factors, which can induce rapid, short-term, and long-term adaptation processes [5,6,7,8,9]
The potential molecular mechanisms underlying these effects included disturbances in redox homeostasis (as evidence by the enhanced production of ROS and reactive nitrogen species), failure of enzymatic and nonenzymatic cytoprotective mechanisms involving the glutathione system as well as nuclear factor kappa B (NF-B) and fibroblast growth factor 2-mediated pathways, and impaired mitochondrial function
Engraftment of severe combined immune deficient mice receiving allogeneic bone marrow via in utero or postnatal transfer
Current single-nucleus RNA-seq datasets from human AD tissue reveal distinct ferroptosis-related transcriptional programs in glial cells, including upregulation of TFRC, FTH1, SLC40A1, and ACSL4, which indicate enhanced iron turnover and lipid peroxidation susceptibility (Leng et al., 2021)
