REVIEW article
Front. Physiol.
Sec. Cardiac Electrophysiology
Volume 16 - 2025 | doi: 10.3389/fphys.2025.1644898
This article is part of the Research TopicExercise Prescription, Physiological Mechanisms, and Exercise Safety in Patients with Cardiac Devices and ArrhythmiasView all articles
Heat Shock Proteins in Atrial Fibrillation: from bench to bedside
Provisionally accepted
- 1Shandong Second Medical University, Weifang, China
- 2Changle County People's Hospital, Weifang, China
- 3Weifang People's Hospital, Weifang, China
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Atrial fibrillation (AF) is the most common age-related arrhythmia in clinic, affecting millions of people around the world, and is closely related to heart failure, ischemic stroke and other diseases. In addition, AF is progressive in nature and represents a significant global health burden. However, the current treatment plans are mainly symptomatic, the efficacy in preventing atrial fibrillation is limited. Hence, there is a pressing need for etiology-specific AF treatments. It is widely acknowledged that the atrial electrical and structural remodeling constitutes the pathological basis of atrial fibrillation. Evidence indicates that heat shock proteins (HSPs) could have a protective effect against AF. HSPs are a diverse family of molecular chaperones that safeguard cells against various stressors. They play a crucial role in mitigating oxidative stress, inflammation, and apoptosis, thereby helping to prevent structural and electrical remodeling in cardiomyocytes. Moreover, HSPs safeguard proteostasis via prevention of toxic protein aggregation by binding to (partially) unfolded proteins. As pivotal inhibitors of AF onset and progression, HSPs represent both a promising therapeutic target and potential biomarkers for staging AF and predicting post-treatment recurrence, as evidenced by recent studies. In this review, we explore the mechanisms of HSP in AF to pave the way for the development of targeted therapies for this prevalent arrhythmia disease.
Keywords: Atrial Fibrillation, Heat shock proteins, Inducer, proteostasis, Inflammation, Oxidative Stress
Received: 11 Jun 2025; Accepted: 14 Jul 2025.
Copyright: © 2025 Zhang, Wang, Nie, Feng, Zhang and Chen. 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: Yanbo Chen, Weifang People's Hospital, Weifang, China
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