Catheter Ablation for Atrial Fibrillation in Cardiac Amyloidosis: A Systematic Review and Meta-Analysis. [PDF]
Sripusanapan A +9 more
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Pre-Amyloidosis Red-Flag Clinical Diagnoses in Light Chain (AL) Versus Age-Related Transthyretin (ATTRwt) Amyloidosis: Electronic Health Record-Based Descriptive Study. [PDF]
Estrada-Merly N +3 more
europepmc +1 more source
Wild-Type Transthyretin Cardiac Amyloidosis Presenting As Progressive Heart Failure and Conduction Disease Despite Guideline-Directed Medical Therapy. [PDF]
Richard S +4 more
europepmc +1 more source
Effect of acoramidis on risk of death and heart problem-related hospitalizations in people with transthyretin amyloid cardiomyopathy: a plain language summary. [PDF]
Judge DP +18 more
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Gene silencing versus protein stabilization in transthyretin amyloid cardiomyopathy: contextualizing the HELIOS-B results and the road to precision agent selection. [PDF]
Khan SA, Ali T, Ul Haque MS, Qamar MA.
europepmc +1 more source
Reply: Causal Inference Challenges in Evaluating Baroreflex Activation Therapy for Transthyretin Amyloid Cardiomyopathy: A Critical Appraisal. [PDF]
Khanna NR +3 more
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Clinical Factors Related to Cardiac Conduction Disturbance in Patients With Wild-Type Transthyretin Amyloid Cardiomyopathy Undergoing Tafamidis Treatment. [PDF]
Hamamoto K +5 more
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Computational Studies on Transthyretin
Among the 23 different fibril proteins described in human amyloidosis, transthyretin is associated with the most common hereditary form of the disease and its knowledge is corroborated through about 150 crystal structures in addition to thousands of small ligands tested as fibril formation inhibitors. In spite of the large amount of available data, the
ORTORE, GABRIELLA MARIA PIA +1 more
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Pathogenesis of transthyretin amyloidosis
Amyloid: the International Journal of Experimental and Clinical Investigation: the Official Journal of the International Society of Amyloidosis, 2012Current dogma for transthyretin (TTR) pathogenesis is that mutations in TTR alter its structure such that the tetramer becomes unstable and prone to release of monomer which then becomes the putative building block of the fibril. This hypothesis is supported by thermodynamic data showing decreased stability of mutant TTR tetrameric proteins and ...
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