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Correction

Correction: Reactive oxygen species and nitric oxide imbalances lead to in vivo and in vitro arrhythmogenic phenotype in acute phase of experimental Chagas disease

  • Artur Santos-Miranda,
  • Julliane Vasconcelos Joviano-Santos,
  • Grazielle Alves Ribeiro,
  • Ana Flávia M. Botelho,
  • Peter Rocha,
  • Leda Quercia Vieira,
  • Jader Santos Cruz,
  • Danilo Roman-Campos
  • Article
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Figs 4 and 5 are switched and are listed under the incorrect legend. Please see the correct figures and legends below.

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Fig 4. Increased action potential (AP) repolarization dispersion and EAD events in PHOX-/- mice during acute chagasic cardiomyopathy.

(A) Four consecutive recorded APs from experimental groups, WT (n = 23); WT 15 days post infection (dpi) (n = 32); PHOX-/- (n = 20) and PHOX-/- 15 dpi (n = 37). EADs are indicated by red arrows. Thirty consecutive APs were analyzed, and the standard deviation (σ) for the time required to reach 90% of AP repolarization was averaged (B) as a measure of AP duration dispersion. (C) Fraction of cells displaying EADs. *p<0.05, compared to WT; #p<0.05, compared to PHOX-/-; &p<0.05, compared to WT 15 dpi. Data were compared using Kruskal-Wallis’ test followed by Dunns’s posttest (B) or Chi-squared test (C); σ: Standard deviation; EAD: Early afterdepolarization; dpi: days post infection. n represents the number of cardiomyocytes.

https://doi.org/10.1371/journal.ppat.1009049.g001

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Fig 5.

ICa-L and IK reduction in peak current density during acute phase of chagasic cardiomyopathy is prevented in PHOX-/- mice (A) Representative IK WT (n = 23); WT 15 days post infection (dpi) (n = 23); PHOX-/- (n = 14) and PHOX-/- 15 dpi (n = 16) and ICa-L (D) traces WT (n = 25); WT 15 days post infection (dpi) (n = 25); PHOX-/- (n = 26) and PHOX-/- 15 dpi (n = 19) recorded from experimental groups. Peak current density from IK (B) and ICa-L (E) were averaged and plotted against membrane potential. Maximum conductance (Gmax) calculated from current-voltage relationship used to normalize the conductance (G) calculated from each tested potential (C and F). No difference in the voltage dependence for channel activation was observed for IK (C) and ICa-L (F). *p<0.05, compared to WT. Data were compared using One way ANOVA’ test followed by Tukey’s posttest dpi: days post infection. n represents the number of cardiomyocytes.

https://doi.org/10.1371/journal.ppat.1009049.g002

Reference

  1. 1. Santos-Miranda A, Joviano-Santos JV, Ribeiro GA, Botelho AFM, Rocha P, Vieira LQ, et al. (2020) Reactive oxygen species and nitric oxide imbalances lead to in vivo and in vitro arrhythmogenic phenotype in acute phase of experimental Chagas disease. PLoS Pathog 16(3): e1008379. https://doi.org/10.1371/journal.ppat.1008379 pmid:32160269

Citation: Santos-Miranda A, Joviano-Santos JV, Ribeiro GA, Botelho AFM, Rocha P, Vieira LQ, et al. (2020) Correction: Reactive oxygen species and nitric oxide imbalances lead to in vivo and in vitro arrhythmogenic phenotype in acute phase of experimental Chagas disease. PLoS Pathog 16(10): e1009049. https://doi.org/10.1371/journal.ppat.1009049

Published: October 28, 2020

Copyright: © 2020 Santos-Miranda et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.