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SHR Neuro Krebs Kardio Lipid Stoffw Microb

Ablasser, K; Verheyen, N; Glantschnig, T; Agnetti, G; Rainer, PP.
Unfolding Cardiac Amyloidosis -From Pathophysiology to Cure.
Curr Med Chem. 2019; 26(16):2865-2878 Doi: 10.2174/0929867325666180104153338
Web of Science PubMed FullText FullText_MUG

 

Führende Autor*innen der Med Uni Graz
Ablasser Klemens
Rainer Peter
Co-Autor*innen der Med Uni Graz
Glantschnig Theresa
Verheyen Nicolas Dominik
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Abstract:
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. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.

Find related publications in this database (Keywords)
Amyloidosis
heart failure
pre-amyloid oligomers
fibrils
immunoglobulin light chains
transthyretin
desmin
posttranslational modification
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