TY - JOUR
T1 - How the endothelium and its bone marrow-derived progenitors influence development of disease
AU - Štefanec, Tihomir
N1 - Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 2004
Y1 - 2004
N2 - The association between diseases accompanied by abnormal endothelial/vascular function (atherosclerosis, hypertension, diabetes mellitus, preeclampsia), and conditions characterized by increased tissue growth and normal endothelial/vascular function (cancer, placental size, birth length, adult height) could be caused by inherited characteristics of endothelial cells and their bone marrow-derived precursors. The genotype responsible for normal endothelial/precursor function could be modified by intrauterine and postnatal endothelial injury; telomere shortening caused by increased endothelial precursor proliferation in response to injury can result in premature endothelial senescence and a decreased precursor proliferative potential, thereby leading to an abnormal endothelial/precursor phenotype and the associated diseases. The individual endothelial/precursor phenotype could be established early in life and its changes in response to risk factors for diseases followed over time, thus providing a unique opportunity for identification and early institution of prophylactic and therapeutic interventions in diseases that cause most of the morbidity and mortality in advanced industrialized societies.
AB - The association between diseases accompanied by abnormal endothelial/vascular function (atherosclerosis, hypertension, diabetes mellitus, preeclampsia), and conditions characterized by increased tissue growth and normal endothelial/vascular function (cancer, placental size, birth length, adult height) could be caused by inherited characteristics of endothelial cells and their bone marrow-derived precursors. The genotype responsible for normal endothelial/precursor function could be modified by intrauterine and postnatal endothelial injury; telomere shortening caused by increased endothelial precursor proliferation in response to injury can result in premature endothelial senescence and a decreased precursor proliferative potential, thereby leading to an abnormal endothelial/precursor phenotype and the associated diseases. The individual endothelial/precursor phenotype could be established early in life and its changes in response to risk factors for diseases followed over time, thus providing a unique opportunity for identification and early institution of prophylactic and therapeutic interventions in diseases that cause most of the morbidity and mortality in advanced industrialized societies.
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U2 - 10.1016/S0306-9877(03)00327-X
DO - 10.1016/S0306-9877(03)00327-X
M3 - Article
C2 - 14962635
AN - SCOPUS:1342289616
SN - 0306-9877
VL - 62
SP - 247
EP - 251
JO - Medical Hypotheses
JF - Medical Hypotheses
IS - 2
ER -