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. 2021 Jan 12;14(1):e007022. doi: 10.1161/CIRCHEARTFAILURE.120.007022

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© 2020 The Authors.

Circulation: Heart Failure is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 7. — Schematic representation of genotype-independent changes in hypertrophic cardiomyopathy (HCM) and genotype-specific differences in the microtubular system. Our analysis shows that all patients with HCM display downregulation of metabolic pathways (electron transport chain [ETC], tricarboxylic acid [TCA] cycle, β-oxidation [β-oxid]) and ribosomal proteins (translation), as well as an upregulation of protein-folding proteins (HSPs [heat shock proteins]) and ECM (extracellular matrix) proteins. HCM_SMP patients have a large increase in microtubules and levels of its detyrosinated form, whereas HCM_SMN patients only have a slight increase compared with nonfailing controls.