Open Access

Redd1 protects against post‑infarction cardiac dysfunction by targeting apoptosis and autophagy

  • Authors:
    • Pianpian Huang
    • Jun Fu
    • Long Chen
    • Chenhui Ju
    • Kefei Wu
    • Hongxia Liu
    • Yun Liu
    • Benming Qi
    • Benling Qi
    • Lihua Liu
  • View Affiliations

  • Published online on: October 4, 2019     https://doi.org/10.3892/ijmm.2019.4366
  • Pages: 2065-2076
  • Copyright: © Huang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Post‑infarction remodeling is accompanied and influenced by perturbations in the mammalian target of rapamycin (mTOR) signaling. Regulated in development and DNA damage response‑1 (Redd1) has been reported to be involved in DNA repair and modulation of mTOR activity. However, little is known about the role of Redd1 in the heart. In the present study the potential contribution of Redd1 overexpression to the chronic phase of heart failure after myocardial infarction (MI) was explored and the mechanisms underlying Redd1 actions were determined. Redd1 was downregulated in the mouse heart subjected to MI surgery. To determine the role of Redd1 in the process of MI, adeno‑associated virus 9 mediated overexpression of Redd1 was used to enhance Redd1 content in cardiomyocytes. Redd1 overexpression improved left ventricular dysfunction and reduced the expansion index. Additionally, Redd1 overexpression resulted in suppressed myocardial apoptosis and improved autophagy. Furthermore, the studies revealed that Redd1 overexpression could inhibit the phosphorylation of mTOR and its downstream effectors P70/S6 kinase and 4EBP1. In conclusion, this study demonstrated that Redd1 overexpression protects against the development and persistence of heart failure post MI by reducing apoptosis and enhancing autophagy via the mTOR signaling pathway. The present study clearly demonstrated that Redd1 is a therapeutic target in the development of heart failure after MI.
View Figures
View References

Related Articles

Journal Cover

December-2019
Volume 44 Issue 6

Print ISSN: 1107-3756
Online ISSN:1791-244X

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Huang P, Fu J, Chen L, Ju C, Wu K, Liu H, Liu Y, Qi B, Qi B, Liu L, Liu L, et al: Redd1 protects against post‑infarction cardiac dysfunction by targeting apoptosis and autophagy . Int J Mol Med 44: 2065-2076, 2019
APA
Huang, P., Fu, J., Chen, L., Ju, C., Wu, K., Liu, H. ... Liu, L. (2019). Redd1 protects against post‑infarction cardiac dysfunction by targeting apoptosis and autophagy . International Journal of Molecular Medicine, 44, 2065-2076. https://doi.org/10.3892/ijmm.2019.4366
MLA
Huang, P., Fu, J., Chen, L., Ju, C., Wu, K., Liu, H., Liu, Y., Qi, B., Qi, B., Liu, L."Redd1 protects against post‑infarction cardiac dysfunction by targeting apoptosis and autophagy ". International Journal of Molecular Medicine 44.6 (2019): 2065-2076.
Chicago
Huang, P., Fu, J., Chen, L., Ju, C., Wu, K., Liu, H., Liu, Y., Qi, B., Qi, B., Liu, L."Redd1 protects against post‑infarction cardiac dysfunction by targeting apoptosis and autophagy ". International Journal of Molecular Medicine 44, no. 6 (2019): 2065-2076. https://doi.org/10.3892/ijmm.2019.4366