The role of SGLT1 in atrial fibrillation and its relationship with endothelial-mesenchymal transition

Zhi-Hong Ning; Xiu-Heng Wang; Hui-Fang Tang; Heng-Jing Hu

doi:10.1016/j.bbrc.2025.151338

The role of SGLT1 in atrial fibrillation and its relationship with endothelial-mesenchymal transition

Biochem Biophys Res Commun. 2025 Jan 13:748:151338. doi: 10.1016/j.bbrc.2025.151338. Online ahead of print.

Authors

Zhi-Hong Ning¹, Xiu-Heng Wang², Hui-Fang Tang¹, Heng-Jing Hu³

Affiliations

¹ The First Affiliated Hospital, Department of Cardiovascular Medicine, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, PR China.
² The First Affiliated Hospital, Department of Medical-record, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, PR China.
³ The First Affiliated Hospital, Department of Cardiovascular Medicine, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, PR China; Department of Cardiovascular Disease and Key Lab for Atherosclerosis of Hunan Province, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, PR China. Electronic address: [email protected].

PMID: 39823893
DOI: 10.1016/j.bbrc.2025.151338

Abstract

Atrial fibrillation (AF) is a prevalent arrhythmia closely associated with atrial fibrosis, posing significant challenges to cardiovascular health. Recent studies have identified the sodium-glucose co-transporter 1 (SGLT1) as a potential key player in the pathophysiology of heart diseases, particularly in the context of AF and atrial fibrosis. This review aims to synthesize current knowledge regarding the mechanisms by which SGLT1 influences the development of AF and atrial fibrosis, with a specific focus on its relationship with endothelial-mesenchymal transition (EMT). By analyzing the latest research findings, this paper discusses how SGLT1 may modulate structural and functional changes in the atria, thereby enhancing our understanding of the underlying mechanisms driving AF.

Keywords: Atrial fibrillation; Atrial fibrosis; Endothelial-mesenchymal transition; SGLT1.

Publication types

Review