Pathogenetic Loop Between Diabetes and Cell Senescence

  1. Roberto Testa, MD1 and
  2. Antonio Ceriello, MD2
  1. 1Gerontological Research, Italian National Research Centre on Aging, Ancona, Italy
  2. 2Centre of Excellence in Diabetes and Endocrinology, University Hospital of Coventry and Warwickshire, University of Warwick, Coventry, U.K
  1. Address correspondence and reprint requests to Prof. Antonio Ceriello, Warwick Medical School, Clinical Science Research Institute, Clinical Science Building, University Hospital–Walsgrave Campus, Clifford Bridge Road, Coventry CV2 2DX, U.K. E-mail: antonio.ceriello{at}

Cell senescence has recently been postulated as an important cause/consequence of type 2 diabetes and its complications. Cellular senescence is defined as a limited ability of human cells to divide, and it becomes evident through phenotypic changes in morphology, gene expression, and function (1). It has long been known that genomic instability, a hallmark of premature aging disorders such as in the Werner syndrome, is associated with type 2 diabetes (2), and, recently, great attention has been paid to the potential impact of vascular cellular senescence on diabetes by means of the study on endothelial progenitor cells (EPCs). EPCs were discovered in 1997. They are derived from bone marrow and are mobilized to the peripheral circulation in response to different stimuli. Defined as circulating immature cells that contribute to vascular homeostasis and compensatory angiogenesis (3), EPCs are able to regenerate injured endothelium, accelerate re-endothelization, and limit the formation of atherosclerotic lesions. Their identification has prompted an explosion of interest regarding their role in the pathogenesis of micro- and macrovascular diseases. Different studies have demonstrated that EPCs are …

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