Epicardial Adipose Tissue-Derived IL-1β Triggers Postoperative Atrial Fibrillation

Frontiers in Cell and Developmental Biology

Maddalena Conte¹  Vincenza Valerio²  Paolo Poggio²  Emanuele Pilato³  Giuseppe Comentale³  Donato Moschetta⁴  Pasquale Campana⁵  Laura Petraglia⁵  Valentina Parisi⁵  Dario Leosco⁵  Annabella Di Mauro⁶  Monica Cantile⁶  Vittoria D’Esposito⁷  Michele Francesco Di Tolla⁷  Serena Romano⁷  Pietro Formisano⁷  Serena Cabaro⁷ 

[1] Casa di Cura San Michele, Maddaloni, Italy;Centro Cardiologico Monzino IRCCS, Milan, Italy;Department of Advanced Biomedical Sciences, University of Naples Federico II, Naples, Italy;Department of Pharmacological and Biomolecular Sciences, University of Milan, Milan, Italy;Department of Translational Medical Sciences, University of Naples Federico II, Naples, Italy;Pathology Unit, INT-IRCCS Fondazione Pascale, Naples, Italy;URT Genomic of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Naples, Italy;

关键词: epicardial adipose tissue;    cytokines;    inflammation;    atrial fibrillation;    fibrosis;    cardiac remodeling;   

DOI  :  10.3389/fcell.2022.893729

来源: DOAJ

【 摘 要 】

Background and aims: Post-operative atrial fibrillation (POAF), defined as new-onset AF in the immediate period after surgery, is associated with poor adverse cardiovascular events and a higher risk of permanent AF. Mechanisms leading to POAF are not completely understood and epicardial adipose tissue (EAT) inflammation could be a potent trigger. Here, we aim at exploring the link between EAT-secreted interleukin (IL)-1β, atrial remodeling, and POAF in a population of coronary artery disease (CAD) patients.Methods: We collected EAT and atrial biopsies from 40 CAD patients undergoing cardiac surgery. Serum samples and EAT-conditioned media were screened for IL-1β and IL-1ra. Atrial fibrosis was evaluated at histology. The potential role of NLRP3 inflammasome activation in promoting fibrosis was explored in vitro by exposing human atrial fibroblasts to IL-1β and IL-18.Results: 40% of patients developed POAF. Patients with and without POAF were homogeneous for clinical and echocardiographic parameters, including left atrial volume and EAT thickness. POAF was not associated with atrial fibrosis at histology. No significant difference was observed in serum IL-1β and IL-1ra levels between POAF and no-POAF patients. EAT-mediated IL-1β secretion and expression were significantly higher in the POAF group compared to the no-POAF group. The in vitro study showed that both IL-1β and IL-18 increase fibroblasts’ proliferation and collagen production. Moreover, the stimulated cells perpetuated inflammation and fibrosis by producing IL-1β and transforming growth factor (TGF)-β.Conclusion: EAT could exert a relevant role both in POAF occurrence and in atrial fibrotic remodeling.

【 授权许可】

Unknown