How the endothelium and its bone marrow-derived progenitors influence development of disease

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)247-251
Number of pages5
JournalMedical Hypotheses
Volume62
Issue number2
DOIs
StatePublished - 2004
Externally publishedYes

Fingerprint

Endothelium
Bone Marrow
Blood Vessels
Telomere Shortening
Phenotype
Wounds and Injuries
Pre-Eclampsia
Atherosclerosis
Diabetes Mellitus
Endothelial Cells
Genotype
Parturition
Hypertension
Morbidity
Mortality
Growth
Neoplasms
Therapeutics

ASJC Scopus subject areas

  • Developmental Biology
  • Medicine(all)
  • Drug Discovery

Cite this

How the endothelium and its bone marrow-derived progenitors influence development of disease. / Stefanec, Tihomir.

In: Medical Hypotheses, Vol. 62, No. 2, 2004, p. 247-251.

Research output: Contribution to journalArticle

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