REVIEW article
Front. Pharmacol.
Sec. Cardiovascular and Smooth Muscle Pharmacology
This article is part of the Research TopicHeart Failure Induced by Non-Cardiac TherapiesView all 5 articles
sAlpha-7 Nicotinic Acetylcholine Receptor: Targeting the interplay between inflammation, Renin-Angiotensin Aldosterone System, and nervous system for the novel treatment of heart failure
Provisionally accepted
Jordan Swiderski1
Laura Kate Gadanec1
Stephen James Hearth2Benjamin Rowlands2
Andrew James Murphy3
Vasso Apostolopoulos4
Anthony Zulli2*- 1Victoria University, Melbourne, Australia
- 2The University of Notre Dame Australia, Sydney, Australia
- 3Baker Heart and Diabetes Institute, Melbourne, Australia
- 4RMIT University, Melbourne, Australia
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
The incidence and prevalence of heart failure (HF) with preserved ejection fraction (HFpEF) continue to rise, yet evidence-based therapy remains limited. Due to the complexity of HFpEF pathology, traditional HF medication has shown inconsistent efficacy in improving clinical outcomes and reducing morbidity. Therefore, highlighting the urgent need for novel interventions. The αlpha-7 nicotinic acetylcholine receptor (α7nAChR) is a central mediator of the cholinergic anti-inflammatory pathway and has emerged as a promising therapeutic target in various conditions, such as sepsis, arthritis, metabolic dysfunction, and atherosclerosis. This review aims to examine the emerging therapeutic potential of α7nAChR in HF and HFpEF pathology, focusing on its protective role in modulating the complex interplay between systemic and cardiovascular inflammation, renin-angiotensin-aldosterone system activation, neurocardiac signaling and metabolic dysfunction.
Keywords: cardiovascular disease, Cholinergic anti-inflammatory pathway, Heart Failure, Hypertension, renin-angiotensin-aldosterone system, α7 nicotinic acetylcholine receptor
Received: 28 Nov 2025; Accepted: 31 Jan 2026.
Copyright: © 2026 Swiderski, Gadanec, Hearth, Rowlands, Murphy, Apostolopoulos and Zulli. 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: Anthony Zulli
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.