Figure 3.

Alterations in pericyte function in disease states. (A) In Alzheimer's disease, β-amyloid removal across the blood-brain barrier slows so β-amyloid aggregates are formed around blood vessels. β-amyloid is toxic to pericytes and produces superoxide (O₂•⁻), which scavenges NO, forming peroxynitrite (ONOO⁻) and constricting vessels. (B) After cerebral ischaemia, the energy supply to an ischaemic region is not fully restored as many capillaries fail to reperfuse due to blockade by polymorphonuclear leukocytes, generation of reactive oxygen species and capillary constriction. (C) In diabetic retinopathy, high glucose levels trigger pericyte apoptosis and capillary malfunction via activation of protein kinase C δ (PKCδ) and p38α mitogen activated protein kinase (p38αK). Reactive oxygen species (ROS) are generated, producing apoptosis via nuclear factor κB (NF-κB) activation and Src homology-2 domain-containing phosphatase-1 (SHP-1) is activated, which inhibits PDGFR-β, decreasing activity of pro-survival pathways and further promoting apoptosis.