Skip to main content

ORIGINAL RESEARCH article

Front. Cardiovasc. Med.
Sec. Heart Failure and Transplantation
Volume 12 - 2025 | doi: 10.3389/fcvm.2025.1531509
This article is part of the Research Topic Outcome-Oriented Approaches to Arrhythmia and Heart Failure Treatment View all 5 articles

Co-administration of isoprenaline and phenylephrine induced a new HFrEF mouse model through activation of both SNS and RAAS

Provisionally accepted
Huimin Su Huimin Su 1Ming Liu Ming Liu 2Siteng Wang Siteng Wang 3Beiduo Tian Beiduo Tian 1Hao Hu Hao Hu 1Li-Kun Ma Li-Kun Ma 1Jianyuan Pan Jianyuan Pan 1*
  • 1 Department of Cardiology, The First Affiliated Hospital of University of Science and Technology of China Anhui Provincial Hospital, Hefei, Anhui Province, China
  • 2 First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang Uyghur Region, China
  • 3 Department of Cardiology, The Second People's Hospital of Hefei, Hefei, Anhui Province, China

The final, formatted version of the article will be published soon.

    The pathogenesis of human heart failure is diverse, and a large number of animal models have emerged to better understand the development of heart failure in humans. Among them, there are several methods of induction in mouse heart failure models, each with its advantages and disadvantages. The use of drug-induced heart failure models has greatly facilitated basic research and reduced the disadvantages of time-consuming and labor-intensive surgical modeling. In our experiments, we used a combination of isoprenaline (ISO) and phenylephrine (PE) for modeling; we aimed to evaluate whether it is superior to conventional drug-induced models, especially those induced by isoprenaline alone. The ISO and PE were administered for 2 weeks by subcutaneous implantation with a micro-osmolar pump, and the mice were monitored dynamically for cardiac ultrasound and blood pressure. RNA sequencing of myocardial tissues after execution of mice further clarified that hypertrophy, fibrosis genes, Sympathetic nervous system (SNS), and Renin-angiotensin-aldosterone system (RAAS) pathways were upregulated. Therefore, we conclude that the ISO/PE-induced mouse heart failure model can activate both the SNS and RAAS, through the activation of both α-adrenergic receptor (α-AR) and β-adrenergic receptor (β-AR), which is more consistent with the development of human heart failure than the ISO-induced model and is expected to be a unique and representative heart failure modeling method.

    Keywords: Heart Failure, Drug Modeling, mouse model, SNS, RAAS

    Received: 20 Nov 2024; Accepted: 03 Feb 2025.

    Copyright: © 2025 Su, Liu, Wang, Tian, Hu, Ma and Pan. 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) or licensor 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.

    * Correspondence: Jianyuan Pan, Department of Cardiology, The First Affiliated Hospital of University of Science and Technology of China Anhui Provincial Hospital, Hefei, 230001, Anhui Province, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.