Two Sod enzymes have been identified in bacteria: a manganese Sod and an iron Sod, encoded by sodA and sodB, respectively. Oxidative stress is potentiated by iron because it reacts with H2O2 in the Fenton reaction. There is increasing evidence of the coordination between the regulation of iron homeostasis and the defences against oxidative stress. Remarkably, SodB is produced exclusively in high iron growth conditions. They can differentiate into mature, functional endothelial-like cells that can be incorporated into vessels and can Albaspidin-AA produce angiogenic factors that contribute to vascular repair and regeneration. Most studies focussed on the exploration of EPCs for therapeutic angiogenesis or the examination of EPCs as potential biomarkers for cardiovascular disease, have used cells that are generated by the culture of peripheral blood mononuclear cells on fibronectin in vascular endothelial growth factor -containing medium. These EPCs are not homogeneous but rather constitute a heterogenic population that mainly originates from myeloid hematopoietic cells. Furthermore, phenotypic analysis has revealed few EPCs expressing stem/progenitor-cell markers. These findings make it controversial to name these cells “EPCs” and the term “CACs” has been suggested, given that these cells have been shown to promote angiogenesis and vascular repair in various experimental settings. We hypothesized that CAC function from patients with HHT is impaired, and can be demonstrated in a series of in vitro cell function assays. ENG and ALK1 have been shown to be essential for the maintenance of endothelial cell morphology and structure. Fernandez et al. have shown that Isochlorogenic-acid-C circulating blood outgrowth endothelial cells derived from patients with HHT appear larger and rounder compared to the characteristic endothelial cobblestone shape of BOECs from control individuals. Furthermore, BOECs from individuals with HHT showed disorganization of the F-actin cytoskeleton, thought to be responsible for increased EC fragility and consequent capillary loss. Vessel injury in HHT patients occurs randomly as a result of inflammation, trauma and other adverse insults, and therefore rapid and efficient repair of the endothelium is critical. CACs contribute to vascular repair through transdifferentiation into ECs as well as through the production of angiogenic growth factors. We demonstrated in this study that CACs from HHT patients not only displayed a disparate morphology, but also had a reduced ability to differentiate to EC linage cells. In addition, mRNA levels of eNOS, an important angiogenic agent, were found to be significantly lower in CACs 
from HHT patients. Predictors of decreased eGFR after two years of ART included older age, lower BMI, and lower CD4 count but, notably, did not include the patient’s baseline eGFR or whether the patient received a tenofovir-containing regimen. In fact, our data showed a nonsignificant trend towards renal improvement in those who received tenofovir-containing regimens. Our findings support the WHO’s 2013 recommendation for a tenofovir-based first-line ART regimen and provide reassurance that, in most patients, tenofovir treatment likely does not require renal monitoring for toxicity.