Reduced apelin expression and atrial fibrosis in postoperative atrial fibrillation following coronary artery bypass grafting
- 1Department of Cardiovascular Surgery, Shanxi Cardiovascular Hospital (Institute), Taiyuan, Shanxi, China
Abstract
The role of apelin in atrial fibrosis linked to postoperative atrial fibrillation (POAF) following coronary artery bypass grafting (CABG) is not fully understood. This exploratory study investigated apelin's association with POAF-related atrial fibrosis and its impact on profibrotic signaling. The study included 18 patients: six CABG patients with POAF, six CABG patients without POAF, and six patients with congenital heart disease in sinus rhythm (serving as a secondary reference). Left atrial appendage tissue was analyzed histologically and molecularly, and serum apelin levels were measured on postoperative day 2 in CABG patients. Primary neonatal rat atrial fibroblasts were treated with transforming growth factor-β1 (TGF-β1) both with and without apelin, or subjected to apelin silencing. Compared with CABG patients without POAF, the POAF group exhibited lower atrial apelin expression and serum concentrations, increased collagen deposition, elevated TGF-β1 expression, and enhanced phosphorylation of mothers against decapentaplegic homolog 2 (Smad2), while total Smad2 remained unchanged. Experimentally, apelin attenuated TGF-β1-induced fibroblast activation, collagen expression, and Smad2 phosphorylation. Conversely, apelin silencing increased the expression of fibrosis-associated proteins. These preliminary findings suggest a link between reduced apelin and atrial fibrosis, as well as POAF after CABG. They also indicate antifibrotic effects of apelin, potentially mediated through TGF-β1/Smad2 signaling. Further research with larger clinical cohorts and complementary experimental models is necessary to fully elucidate the pathway mediation and clinical significance of these findings.
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BibTeX
@article{xu2026reduced,
title = {{Reduced apelin expression and atrial fibrosis in postoperative atrial fibrillation following coronary artery bypass grafting}},
author = {Yijun Xu and Zhiqiang Chen and Peng Liu and Wen Wen and Xiaowei Li and Hao Wang},
journal = {Biomolecules \& Biomedicine},
year = {2026},
month = nov,
doi = {10.17305/bb.2026.14946},
url = {https://doi.org/10.17305/bb.2026.14946},
note = {CC BY},
}
RIS
TY - JOUR
TI - Reduced apelin expression and atrial fibrosis in postoperative atrial fibrillation following coronary artery bypass grafting
AU - Yijun Xu
AU - Zhiqiang Chen
AU - Peng Liu
AU - Wen Wen
AU - Xiaowei Li
AU - Hao Wang
PY - 2026
DA - 2026/11/06
JO - Biomolecules & Biomedicine
DO - 10.17305/bb.2026.14946
UR - https://doi.org/10.17305/bb.2026.14946
AB - The role of apelin in atrial fibrosis linked to postoperative atrial fibrillation (POAF) following coronary artery bypass grafting (CABG) is not fully understood. This exploratory study investigated apelin's association with POAF-related atrial fibrosis and its impact on profibrotic signaling. The study included 18 patients: six CABG patients with POAF, six CABG patients without POAF, and six patients with congenital heart disease in sinus rhythm (serving as a secondary reference). Left atrial appendage tissue was analyzed histologically and molecularly, and serum apelin levels were measured on postoperative day 2 in CABG patients. Primary neonatal rat atrial fibroblasts were treated with transforming growth factor-β1 (TGF-β1) both with and without apelin, or subjected to apelin silencing. Compared with CABG patients without POAF, the POAF group exhibited lower atrial apelin expression and serum concentrations, increased collagen deposition, elevated TGF-β1 expression, and enhanced phosphorylation of mothers against decapentaplegic homolog 2 (Smad2), while total Smad2 remained unchanged. Experimentally, apelin attenuated TGF-β1-induced fibroblast activation, collagen expression, and Smad2 phosphorylation. Conversely, apelin silencing increased the expression of fibrosis-associated proteins. These preliminary findings suggest a link between reduced apelin and atrial fibrosis, as well as POAF after CABG. They also indicate antifibrotic effects of apelin, potentially mediated through TGF-β1/Smad2 signaling. Further research with larger clinical cohorts and complementary experimental models is necessary to fully elucidate the pathway mediation and clinical significance of these findings.
SN - 2831-0896
SN - 2831-090X
ER -