Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
Landiolol attenuates atrial remodeling in septic rats by upregulating calumenin
Zhi-Hui He, Lian-Kui Wu, Hao Liu, Ling-Yu Bai, Jian-Jun Du, Kui-Ying Ma, Yu Wang, Ming Zhao
Zhi-Hui He, School of Basic Medical Sciences, Inner Mongolia Minzu University, Tongliao 028000, Inner Mongolia Autonomous Region, China
Lian-Kui Wu, Intensive Care Unit, Affiliated Hospital of Inner Mongolia Minzu University, Tongliao 028000, Inner Mongolia Autonomous Region, China
Hao Liu, Section of Anatomy, Inner Mongolia Minzu University, Tongliao 028000, Inner Mongolia Autonomous Region, China
Ling-Yu Bai, Kui-Ying Ma, Ming Zhao, Department of Cardiovascular Medicine, Affiliated Hospital of Inner Mongolia Minzu University, Tongliao 028000, Inner Mongolia Autonomous Region, China
Jian-Jun Du, Department of Cardiovascular Medicine, The First People’s Hospital of Horqin District, Tongliao 028000, Inner Mongolia Autonomous Region, China
Yu Wang, Key Laboratory of Basic Pharmacology of the Ministry of Education, Zunyi Medical University, Zunyi 563000, Guizhou Province, China
Co-corresponding authors: Yu Wang and Ming Zhao.
Author contributions: He ZH conducted the research, investigation, formal analysis, and writing original draft; Wu LK contributed to investigation, conceptualization, and methodology; Liu H contributed to validation, visualization, and formal analysis; Bai LY, Du JJ and Ma KY contributed to data curation, and formal analysis; Wang Y and Zhao M designed the research, and contributed to formal analysis, project administration, and writing review and editing, contributed equally to this study as co-corresponding authors; all authors have read and approved the final version to be published.
AI contribution statement: All the research content, academic viewpoints, experimental data and professional terminology remain unchanged and unused AI.
Supported by Natural Science Foundation of Inner Mongolia Autonomous Region of China, No. 2023LHMS08082, No. 2018MS08036, and No. 2021MS08069; and Scientific Research in Higher Education Institutions of the Inner Mongolia Autonomous Region, China, No. NJZY22456.
Institutional animal care and use committee statement: This study was approved by the Medical Ethics Committee of Affiliated Hospital of Inner Mongolia Minzu University (approval No. NM-LL-2024-04-01-36).
Conflict-of-interest statement: All authors declare no conflict of interest in publishing the manuscript.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Data sharing statement: No additional data are available.
Corresponding author: Ming Zhao, PhD, Chief Physician, Department of Cardiovascular Medicine, Affiliated Hospital of Inner Mongolia Minzu University, No. 22 Holin He Street, Tongliao 028000, Inner Mongolia Autonomous Region, China.
langzhe73@163.com
Received: February 24, 2026
Revised: March 13, 2026
Accepted: May 28, 2026
Published online: July 26, 2026
Processing time: 153 Days and 3.9 Hours
BACKGROUND
As a crucial pathological event during sepsis progression, atrial electrical remodeling markedly exacerbates disease severity. The associated high mortality and morbidity rates present a severe threat to patients’ survival and well-being.
AIM
To investigate the effects and mechanisms of the ultrashort-acting β-blocker landiolol on atrial electrical and structural remodeling in septic rats.
METHODS
A rat model of sepsis was established. The effects of landiolol on right atrial conduction time, conduction velocity, conduction dispersion, and basic electrophysiological parameters (PR interval, heart rate) were assessed using electrical mapping technology. Myocardial inflammatory injury was observed via hematoxylin and eosin staining, serum levels of inflammatory cytokines were measured by enzyme-linked immunosorbent assay, and myocardial fibrosis was evaluated using Masson staining. Apoptosis and endoplasmic reticulum stress-related proteins: Glucose-regulated protein 78 and C/EBP homologous protein were detected by immunofluorescence, immunohistochemistry, and Western blot. The expression of calumenin was examined by immunohistochemistry and Western blot.
RESULTS
Landiolol partially ameliorated sepsis-induced prolongation of atrial conduction time, decreased conduction velocity, increased conduction dispersion, and altered PR interval. Landiolol significantly attenuated myocardial inflammatory cell infiltration, necrosis, and elevated serum levels of tumor necrosis factor-α and interleukin-6 induced by sepsis. It also improved collagen deposition and fibrosis in the myocardium and reduced endoplasmic reticulum stress-induced apoptosis. Furthermore, landiolol significantly upregulated the expression of calumenin protein.
CONCLUSION
Landiolol may protect myocardium by upregulating calumenin expression, thereby alleviating electrical and structural remodeling in septic rats. This study provides evidence for the use of landiolol in alleviating atrial remodeling.
Core Tip: This study first established a sepsis rat model and validated the modeling success by detecting elevated serum inflammatory cytokine levels using enzyme-linked immunosorbent assay. The model was treated with landiolol to compare the degree of inflammatory injury, myocardial fibrosis, and changes in atrial electrophysiology among the different groups. Immunofluorescence, immunohistochemistry, and Western blot analyses were performed to detect the expression of apoptosis-related proteins and endoplasmic reticulum stress-related proteins (glucose-regulated protein 78 and C/EBP homologous protein) and calumenin. The results indicated that landiolol may protect the myocardium by upregulating calumenin expression, thereby mitigating atrial electrical and structural remodeling in sepsis rats.
