Senescence and extracellular vesicles: novel partners in vascular amyloidosis

Meredith Whitehead, Marco Antonazzi, Catherine M. Shanahan*

*Corresponding author for this work

Research output: Contribution to journalEditorialpeer-review

1 Citation (Scopus)


Amyloidosis is a prevalent age-associated pathology caused by the accumulation of fibrous, insoluble protein fibrils in tissues. The most common human amyloid is aortic medial amyloid (AMA), caused by aggregation of a 50-amino acid peptide called medin, which is cleaved by an unknown mechanism from its parent protein, milk fat globulin EGF-factor 8 (MFGE8). Medin is present in the vessel wall of 97% of Caucasians aged over 50-years, yet despite its prevalence in the ageing population there is a very limited understanding of the mechanisms driving AMA. The novel data presented in the paper by Whitehead et al. provides evidence that vascular smooth muscle cell (VSMC)-derived small extracellular vesicles (sEVs) are key mediators of medin accumulation in the vessel wall [1]. In addition, the authors identify, for the first time, a role for cellular senescence in triggering amyloidosis via changes in sEVs and extracellular matrix (ECM) composition.

Original languageEnglish
Pages (from-to)1232-1234
Number of pages3
Issue number5
Early online date1 Mar 2023
Publication statusPublished - 15 Mar 2023


  • amyloid
  • extracellular vesicles
  • medin
  • senescence
  • smooth muscle cells


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