The emerging role of Notch pathway in ageing: Focus on the related mechanisms in age-related diseases

Carmela Rita Balistreri, Rosalinda Madonna, Gerry Melino, Calogero Caruso

Research output: Contribution to journalReview articlepeer-review

Abstract

Notch signaling is an evolutionarily conserved pathway, which is fundamental for the development of all tissues, organs and systems of human body. Recently, a considerable and still growing number of studies have highlighted the contribution of Notch signaling in various pathological processes of the adult life, such as age-related diseases. In particular, the Notch pathway has emerged as major player in the maintenance of tissue specific homeostasis, through the control of proliferation, migration, phenotypes and functions of tissue cells, as well as in the cross-talk between inflammatory cells and the innate immune system, and in onset of inflammatory age-related diseases. However, until now there is a confounding evidence about the related mechanisms. Here, we discuss mechanisms through which Notch signaling acts in a very complex network of pathways, where it seems to have the crucial role of hub. Thus, we stress the possibility to use Notch pathway, the related molecules and pathways constituting this network, both as innovative (predictive, diagnostic and prognostic) biomarkers and targets for personalised treatments for age-related diseases.

Original languageEnglish
Pages (from-to)50-65
Number of pages16
JournalAgeing Research Reviews
Volume29
DOIs
Publication statusPublished - Aug 1 2016

Keywords

  • A signaling complex network
  • Age-related diseases
  • Ageing
  • Biomarkers and targets for personalized treatments
  • Involved mechanisms
  • Notch pathway

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Ageing
  • Molecular Biology
  • Neurology

Fingerprint Dive into the research topics of 'The emerging role of Notch pathway in ageing: Focus on the related mechanisms in age-related diseases'. Together they form a unique fingerprint.

Cite this