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. 2022 Nov 10;9:1038114. doi: 10.3389/fcvm.2022.1038114

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Copyright © 2022 MacDonnell, Megna, Ruan, Zhu, Halasz, Jasewicz, Powers, E, del Pilar Molina-Portela, Jin, Zhang, Torello, Feric, Graziano, Shekhar, Dunn, Glass and Morton.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Activin A overexpression in mice produced cardiac dysfunction. Comparison of physical and molecular characteristics in control and Activin A–treated mice. (A) In vivo circulating levels of Activin A. (B) Heart-to-body weight ratio. (C) Circulating NT-proANP. (D) Gene expression in LV + S tissue. (E) Pressure-volume loop analyses. Statistical analyses were performed using an unpaired two-tailed t-test. *P < 0.05, **P < 0.01. ActA, Activin A; ESPVR, end systolic pressure–volume relationship; HDD, hydrodynamic delivery; LV + S, left ventricle and septum; NT-proANP, N-terminal pro-atrial natriuretic peptide.