Nature Communications (Dec 2021)
Plasmin activity promotes amyloid deposition in a transgenic model of human transthyretin amyloidosis
- Ivana Slamova,
- Rozita Adib,
- Stephan Ellmerich,
- Michal R. Golos,
- Janet A. Gilbertson,
- Nicola Botcher,
- Diana Canetti,
- Graham W. Taylor,
- Nigel Rendell,
- Glenys A. Tennent,
- Guglielmo Verona,
- Riccardo Porcari,
- P. Patrizia Mangione,
- Julian D. Gillmore,
- Mark B. Pepys,
- Vittorio Bellotti,
- Philip N. Hawkins,
- Raya Al-Shawi,
- J. Paul Simons
Affiliations
- Ivana Slamova
- Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, University College London
- Rozita Adib
- Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, University College London
- Stephan Ellmerich
- Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, University College London
- Michal R. Golos
- Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, University College London
- Janet A. Gilbertson
- Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, University College London
- Nicola Botcher
- Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, University College London
- Diana Canetti
- Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, University College London
- Graham W. Taylor
- Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, University College London
- Nigel Rendell
- Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, University College London
- Glenys A. Tennent
- Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, University College London
- Guglielmo Verona
- Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, University College London
- Riccardo Porcari
- Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, University College London
- P. Patrizia Mangione
- Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, University College London
- Julian D. Gillmore
- Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, University College London
- Mark B. Pepys
- Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, University College London
- Vittorio Bellotti
- Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, University College London
- Philip N. Hawkins
- Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, University College London
- Raya Al-Shawi
- Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, University College London
- J. Paul Simons
- Centre for Amyloidosis and Acute Phase Proteins, Division of Medicine, University College London
- DOI
- https://doi.org/10.1038/s41467-021-27416-z
- Journal volume & issue
-
Vol. 12,
no. 1
pp. 1 – 13
Abstract
ATTR amyloidosis causes heart failure through the accumulation of misfolded transthyretin in cardiac muscle. Here the authors report a mouse model of ATTR amyloidosis and demonstrate the involvement of protease activity in ATTR amyloid deposition.
