New Insights on Premature Aging Diseases and Links to Aging and Cancer

Dear Colleagues,

The global population is projected to increase in the coming years, and the median survival age will continue to increase. Aging is thus becoming both a demographic and a socio-economic challenge in many countries since it is a major risk factor for the development of age-related morbidities such as cancer, cardiovascular disorders, and neurodegenerative diseases. On the other hand, cancer is one of the most frequent causes of death in developed countries.

Premature aging or progeroid syndromes (PS) are rare genetic diseases characterized by a premature aging phenotype largely mimicking physiological aging. Most of them are caused by defects of genes encoding nuclear matrix or DNA repair proteins, which are among the major hallmarks of aging at the cellular and molecular levels, in relation to cellular senescence. In addition, many PS share a common mechanistic basis, as they are associated to a defective prenylated protein, being either accumulated or activated. This is the case in classical Hutchinson–Gilford progeria and related PS (restrictive dermopathy, mandibuloacral dysplasia type B, etc.) where prenylated progerin or prelamin A accumulates in the cells’ nuclei, exerting toxic effects on several fundamental nuclear functions, being the key mechanism leading to the clinical symptoms. Interestingly, progerin has been found to be accumulated in aged tissues of healthy individuals, suggesting its contribution to physiological aging. Besides, several other PS have been discovered as being caused by activating mutations in genes encoding permanently prenylated proteins of the RAS-MAPK pathways. In these RASopathies, such as Costello or Noonan syndromes, H-RAS or K-RAS are mutated.

Mechanistic links between cellular proliferation and senescence have been demonstrated for a long time, further providing clues towards a biological and clinical balance between aging and cancer. Cellular senescence that contributes to organismal aging is an essential tumor-suppressor mechanism. Defective prelamin A processing or DNA repair mechanisms, defective MAPK pathways, being involved in PS, are also major players of tumor-cell proliferation.

This Special Issue provides the opportunity to publish original research and review articles in the exciting field of premature aging syndromes, and their molecular links with natural aging and cancer. We would like to invite articles that address the application of molecular and cell biology together with living models to cancer and aging research, from the identification of new pathophysiological mechanisms or biomarkers to the identification of therapeutic proofs of principle, paving the way to new therapies in these fields.

Prof. Dr. Nicolas Levy
Prof. Dr. Patrice Roll
Guest Editors

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