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Larixyl acetate, a TRPC6 inhibitor, attenuates pressure overload‑induced heart failure in mice

  • Authors:
    • Min Jia
    • Wenxue Liu
    • Keyin Zhang
    • Zhigang Wang
    • Ruisha Li
    • Jun Pan
    • Jianjun Yang
    • Dongjin Wang
  • View Affiliations / Copyright

    Affiliations: Department of Anesthesiology, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Zhengzhou, Henan 450052, P.R. China, Department of Cardiothoracic Surgery, Institute of Cardiothoracic Vascular Disease, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu 210000, P.R. China
    Copyright: © Jia et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 49
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    Published online on: January 25, 2024
       https://doi.org/10.3892/mmr.2024.13174
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Abstract

Heart failure is a primary cause of global mortality. In the present study, whether larixyl acetate, an inhibitor of transient receptor potential cation channel subfamily C member 6, attenuates pressure overload‑induced heart failure in mice was investigated. To test this hypothesis, a transverse aortic constriction (TAC) animal model and an angiotensin II (Ang II)‑treated H9c2 cell model were used. Cardiac and cellular structure, function and the expression levels of hypertrophy, endoplasmic reticulum (ER) stress, apoptosis, autophagy and pmTOR/mTOR related mRNAs or proteins were assessed to explore the underlying molecular mechanisms. The results indicated that treatment with TAC or Ang II leads to significant hypertrophy and dysfunction of the heart or H9c2 cells, accompanied by an increase in ER stress, apoptosis and activation of the mTOR signaling pathway, and a decrease in autophagy. The administration of larixyl acetate attenuated these impairments, which can be reversed by inhibiting autophagy through the activation of the mTOR signaling pathway. These findings suggested that larixyl acetate can effectively protect against pressure overload‑induced heart failure by enhancing autophagy and limiting ER stress and apoptosis through inhibition of the mTOR pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Jia M, Liu W, Zhang K, Wang Z, Li R, Pan J, Yang J and Wang D: Larixyl acetate, a TRPC6 inhibitor, attenuates pressure overload‑induced heart failure in mice. Mol Med Rep 29: 49, 2024.
APA
Jia, M., Liu, W., Zhang, K., Wang, Z., Li, R., Pan, J. ... Wang, D. (2024). Larixyl acetate, a TRPC6 inhibitor, attenuates pressure overload‑induced heart failure in mice. Molecular Medicine Reports, 29, 49. https://doi.org/10.3892/mmr.2024.13174
MLA
Jia, M., Liu, W., Zhang, K., Wang, Z., Li, R., Pan, J., Yang, J., Wang, D."Larixyl acetate, a TRPC6 inhibitor, attenuates pressure overload‑induced heart failure in mice". Molecular Medicine Reports 29.3 (2024): 49.
Chicago
Jia, M., Liu, W., Zhang, K., Wang, Z., Li, R., Pan, J., Yang, J., Wang, D."Larixyl acetate, a TRPC6 inhibitor, attenuates pressure overload‑induced heart failure in mice". Molecular Medicine Reports 29, no. 3 (2024): 49. https://doi.org/10.3892/mmr.2024.13174
Copy and paste a formatted citation
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Spandidos Publications style
Jia M, Liu W, Zhang K, Wang Z, Li R, Pan J, Yang J and Wang D: Larixyl acetate, a TRPC6 inhibitor, attenuates pressure overload‑induced heart failure in mice. Mol Med Rep 29: 49, 2024.
APA
Jia, M., Liu, W., Zhang, K., Wang, Z., Li, R., Pan, J. ... Wang, D. (2024). Larixyl acetate, a TRPC6 inhibitor, attenuates pressure overload‑induced heart failure in mice. Molecular Medicine Reports, 29, 49. https://doi.org/10.3892/mmr.2024.13174
MLA
Jia, M., Liu, W., Zhang, K., Wang, Z., Li, R., Pan, J., Yang, J., Wang, D."Larixyl acetate, a TRPC6 inhibitor, attenuates pressure overload‑induced heart failure in mice". Molecular Medicine Reports 29.3 (2024): 49.
Chicago
Jia, M., Liu, W., Zhang, K., Wang, Z., Li, R., Pan, J., Yang, J., Wang, D."Larixyl acetate, a TRPC6 inhibitor, attenuates pressure overload‑induced heart failure in mice". Molecular Medicine Reports 29, no. 3 (2024): 49. https://doi.org/10.3892/mmr.2024.13174
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