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Adzika GK, Hou H, Adekunle AO, et al. Amlexanox and Forskolin Prevents Isoproterenol-Induced Cardiomyopathy by Subduing Cardiomyocyte Hypertrophy and Maladaptive Inflammatory Responses. Front Cell Dev Biol. 2021;9:719351doi: 10.3389/fcell.2021.719351.
Adzika, G. K., Hou, H., Adekunle, A. O., Rizvi, R., Adzraku, S. Y., Li, K., Deng, Q. M., Mprah, R., Ndzie Noah, M. L., Adu-Amankwaah, J., Machuki, J. O., Shang, W., Ma, T., Koda, S., Ma, X., & Sun, H. (2021). Amlexanox and Forskolin Prevents Isoproterenol-Induced Cardiomyopathy by Subduing Cardiomyocyte Hypertrophy and Maladaptive Inflammatory Responses. Frontiers in cell and developmental biology, 9719351. https://doi.org/10.3389/fcell.2021.719351
Adzika, Gabriel Komla, et al. "Amlexanox and Forskolin Prevents Isoproterenol-Induced Cardiomyopathy by Subduing Cardiomyocyte Hypertrophy and Maladaptive Inflammatory Responses." Frontiers in cell and developmental biology vol. 9 (2021): 719351. doi: https://doi.org/10.3389/fcell.2021.719351
Adzika GK, Hou H, Adekunle AO, Rizvi R, Adzraku SY, Li K, Deng QM, Mprah R, Ndzie Noah ML, Adu-Amankwaah J, Machuki JO, Shang W, Ma T, Koda S, Ma X, Sun H. Amlexanox and Forskolin Prevents Isoproterenol-Induced Cardiomyopathy by Subduing Cardiomyocyte Hypertrophy and Maladaptive Inflammatory Responses. Front Cell Dev Biol. 2021 Sep 24;9:719351. doi: 10.3389/fcell.2021.719351. eCollection 2021. PMID: 34631707; PMCID: PMC8497899.
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Front Cell Dev Biol. 2021 Sep 24;9:719351. doi: 10.3389/fcell.2021.719351. eCollection 2021.

Amlexanox and Forskolin Prevents Isoproterenol-Induced Cardiomyopathy by Subduing Cardiomyocyte Hypertrophy and Maladaptive Inflammatory Responses.

Frontiers in cell and developmental biology

Gabriel Komla Adzika, Hongjian Hou, Adebayo Oluwafemi Adekunle, Ruqayya Rizvi, Seyram Yao Adzraku, Kexue Li, Qi-Ming Deng, Richard Mprah, Marie Louise Ndzie Noah, Joseph Adu-Amankwaah, Jeremiah Ong'achwa Machuki, Wenkang Shang, Tongtong Ma, Stephane Koda, Xianluo Ma, Hong Sun

Affiliations

  1. Department of Physiology, Xuzhou Medical University, Xuzhou, China.
  2. The College of Biology and Food, Shangqiu Normal University, Shangqiu, China.
  3. Xuzhou Medical University, Xuzhou, China.
  4. Key Laboratory of Bone Marrow Stem Cell, Department of Hematology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.
  5. The Key Laboratory of Cardiovascular Remodeling and Function Research, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Chinese Ministry of Education, Department of Cardiology, Chinese National Health Commission and Chinese Academy of Medical Sciences, Qilu Hospital of Shandong University, Jinan, China.
  6. Faculty of Biology, Institute of Biochemistry and Molecular Biology, ZBMZ, Albert-Ludwigs University of Freiburg, Freiburg, Germany.
  7. Laboratory of Infection and Immunity, Department of Pathogenic Biology and Immunology, Xuzhou Medical University, Xuzhou, China.
  8. Internal Medicine-Cardiovascular Department, People's Hospital of Jiawang District, Xuzhou, China.

PMID: 34631707 PMCID: PMC8497899 DOI: 10.3389/fcell.2021.719351

Abstract

Chronic catecholamine stress (CCS) induces the occurrence of cardiomyopathy-pathological cardiac hypertrophy (PCH), which is characterized by left ventricular systolic dysfunction (LVSD). Recently, mounting evidence has implicated myocardial inflammation in the exacerbation of pathological cardiac remodeling. However, there are currently no well-defined treatment interventions or regimes targeted at both the attenuation of maladaptive myocardial hypertrophy and inflammation during CCS to prevent PCH. G protein-coupled receptor kinase 5 (GRK5) and adenylyl cyclases (ACs)-cAMP mediates both cardiac and inflammatory responses. Also, GRK5 and ACs are implicated in stress-induced LVSD. Herein, we aimed at preventing PCH during CCS via modulating adaptive cardiac and inflammatory responses by inhibiting GRK5 and/or stimulating ACs. Isoproterenol-induced cardiomyopathy (ICM) was modeled using 0.5 mg/100 g/day isoproterenol injections for 40 days. Alterations in cardiac and inflammatory responses were assessed from the myocardia. Similarities in the immunogenicity of cardiac troponin I (cTnI) and lipopolysaccharide under CCS were assessed, and Amlexanox (35 μM/ml) and/or Forskolin (10 μM/ml) were then employed

Copyright © 2021 Adzika, Hou, Adekunle, Rizvi, Adzraku, Li, Deng, Mprah, Ndzie Noah, Adu-Amankwaah, Machuki, Shang, Ma, Koda, Ma and Sun.

Keywords: GRK5; adenylyl cyclase; amlexanox; cAMP; chronic catecholamine stress; forskolin; inflammation; isoproterenol-induced cardiomyopathy

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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