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Start Over Author "Glantschnig, Theresa" Topic amyloid neuropathies, familial
2 results on '"Glantschnig, Theresa"'

1. Unfolding Cardiac Amyloidosis -From Pathophysiology to Cure.

Author

Ablasser K, Verheyen N, Glantschnig T, Agnetti G, and Rainer PP

Subjects
Amyloid Neuropathies, Familial physiopathology, Amyloid Neuropathies, Familial therapy, Animals, Heart Diseases physiopathology, Heart Diseases therapy, Humans, Immunoglobulin Light Chains metabolism, Immunoglobulin Light-chain Amyloidosis physiopathology, Immunoglobulin Light-chain Amyloidosis therapy, Immunotherapy, Liver Transplantation, Prealbumin metabolism, Protein Multimerization drug effects, Stem Cell Transplantation, Amyloid Neuropathies, Familial drug therapy, Heart Diseases drug therapy, Immunoglobulin Light-chain Amyloidosis drug therapy
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.)

Published
2019
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2. Unfolding Cardiac Amyloidosis - From Pathophysiology to Cure

Author

Klemens Ablasser, Theresa Glantschnig, Peter P. Rainer, Giulio Agnetti, Nicolas Verheyen, Ablasser, Klemen, Verheyen, Nicola, Glantschnig, Theresa, Agnetti, Giulio, and Rainer, Peter P

Subjects
medicine.medical_specialty, Heart Diseases, Pre-amyloid oligomer, Disease, 030204 cardiovascular system & hematology, Biochemistry, Transthyretin, Desmin, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Drug Discovery, medicine, Amyloidosi, Posttranslational Modification, Animals, Humans, Prealbumin, Immunoglobulin Light-chain Amyloidosis, 030304 developmental biology, Fibril, Pharmacology, Heart Failure, 0303 health sciences, Amyloid Neuropathies, Familial, biology, business.industry, Amyloidosis, Organic Chemistry, medicine.disease, Pathophysiology, Liver Transplantation, Amyloid deposition, Cardiac amyloidosis, Heart failure, Cardiology, biology.protein, cardiovascular system, Molecular Medicine, Immunoglobulin Light Chains, Immunotherapy, Immunoglobulin Light Chain, Protein Multimerization, business, Stem Cell Transplantation
Abstract

Deposition of amyloidogenic proteins leading to the formation of amyloid fibrils in the myocardium cause 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. The reversal or arrest of adverse cardiac remodeling is the target of current therapies, as cardiac-related mortality worsens prognosis in patients where the underlying systemic amyloidosis was successfully treated. 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 touch on acquired amyloid deposition in cardiovascular disease other than AL or ATTR.

Published
2019

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