Cardiac amyloidosis (CA) is an infiltrative disease caused by progressive deposition of amyloid fibres in the heart. The most common forms include immunoglobulin light-chain and transthyretin amyloidosis. Current therapies for CA either stabilize or block the production of amyloidogenic precursors, preventing further amyloid deposition. This approach, while reducing cell damage and disease progression, does not target pre-existing amyloid deposits. Conversely, amyloid removal might stimulate functional recovery of the affected organ, thus improving quality of life and survival. A therapeutic strategy based on monoclonal antibodies capable of selectively binding amyloid deposits and inducing their removal has recently been tested in various clinical trial, with promising results, and could represent a key treatment for CA in the near future.
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Harvard Med Sch, Brigham & Womens Hosp, Dept Med, Div Genet, Boston, MA 02115 USAHarvard Med Sch, Brigham & Womens Hosp, Dept Med, Div Genet, Boston, MA 02115 USA
Joshi, Shaurya
Evangelisti, Alessandro
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Stanford Univ, Sch Med, Stanford Cardiovasc Inst, Stanford, CA 94305 USA
Stanford Univ, Sch Med, Div Cardiovasc Med, Stanford Amyloid Ctr, 1651 Page Mill Rd,Room 2330, Palo Alto, CA 94304 USAHarvard Med Sch, Brigham & Womens Hosp, Dept Med, Div Genet, Boston, MA 02115 USA
Evangelisti, Alessandro
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Liao, Ronglih
Alexander, Kevin M.
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Stanford Univ, Sch Med, Stanford Cardiovasc Inst, Stanford, CA 94305 USA
Stanford Univ, Sch Med, Div Cardiovasc Med, Stanford Amyloid Ctr, 1651 Page Mill Rd,Room 2330, Palo Alto, CA 94304 USAHarvard Med Sch, Brigham & Womens Hosp, Dept Med, Div Genet, Boston, MA 02115 USA