Unfolding Cardiac Amyloidosis -From Pathophysiology to Cure.
Amyloid Neuropathies, Familial
/ drug therapy
Animals
Heart Diseases
/ drug therapy
Humans
Immunoglobulin Light Chains
/ metabolism
Immunoglobulin Light-chain Amyloidosis
/ drug therapy
Immunotherapy
Liver Transplantation
Prealbumin
/ metabolism
Protein Multimerization
/ drug effects
Stem Cell Transplantation
Amyloidosis
desmin
fibrils
heart failure
immunoglobulin light chains
posttranslational modification
pre-amyloid oligomers
transthyretin.
Journal
Current medicinal chemistry
ISSN: 1875-533X
Titre abrégé: Curr Med Chem
Pays: United Arab Emirates
ID NLM: 9440157
Informations de publication
Date de publication:
2019
2019
Historique:
received:
24
10
2017
revised:
04
12
2017
accepted:
06
12
2017
pubmed:
6
1
2018
medline:
29
10
2019
entrez:
6
1
2018
Statut:
ppublish
Résumé
Deposition of amyloidogenic proteins leading to the formation of amyloid fibrils in the myocardium causes cardiac amyloidosis. Although any form of systemic amyloidosis can affect the heart, light-chain (AL) or transthyretin amyloidosis (ATTR) account for the majority of diagnosed cardiac amyloid deposition. The extent of cardiac disease independently predicts mortality. Thus, the reversal of arrest of adverse cardiac remodeling is the target of current therapies. Here, we provide a condensed overview on the pathophysiology of AL and ATTR cardiac amyloidoses and describe treatments that are currently used or investigated in clinical or preclinical trials. We also briefly discuss acquired amyloid deposition in cardiovascular disease other than AL or ATTR.
Identifiants
pubmed: 29303069
pii: CMC-EPUB-87724
doi: 10.2174/0929867325666180104153338
doi:
Substances chimiques
Immunoglobulin Light Chains
0
Prealbumin
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
2865-2878Informations de copyright
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