TY - JOUR
T1 - Senescence and extracellular vesicles
T2 - novel partners in vascular amyloidosis
AU - Whitehead, Meredith
AU - Antonazzi, Marco
AU - Shanahan, Catherine M.
N1 - Funding Information:
BHF Programme Grant RG/F/21/110064 and FS/19/58/34895
Publisher Copyright:
© 2023 Whitehead et al. This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
PY - 2023/3/15
Y1 - 2023/3/15
N2 - 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.
AB - 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.
KW - amyloid
KW - extracellular vesicles
KW - medin
KW - senescence
KW - smooth muscle cells
UR - https://www.scopus.com/pages/publications/85150751345
U2 - 10.18632/aging.204571
DO - 10.18632/aging.204571
M3 - Editorial
C2 - 36863314
AN - SCOPUS:85150751345
SN - 1945-4589
VL - 15
SP - 1232
EP - 1234
JO - Aging
JF - Aging
IS - 5
ER -