Related Experiment Video
Updated: Jan 13, 2026

08:10
Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation
Published on: July 20, 2022
2.1K
From Tissue to Transcriptome: A Systematic Review of Multi-Level Evidence for Immune Dysregulation in Atrial
Antonio da Silva Menezes Junior1,2, Isabela Jubé Wastowski3, Henrique Lima de Oliveira1
1Internal Medicine, Faculty of Medicine, Federal University of Goiás, Goiânia 74690-900, Brazil.
Journal of Clinical Medicine
|October 29, 2025
Summary
Immune dysregulation, involving T cells and inflammation, drives atrial fibrillation (AF) development and progression. Integrating immune biomarkers may improve risk prediction and guide new AF therapies.
Area of Science:
- Cardiology
- Immunology
- Genetics
Background:
- Immune dysregulation is increasingly recognized as a key factor in atrial fibrillation (AF).
- Evidence implicates T-cell subsets, cellular senescence, checkpoint dysfunction, and inflammatory signaling in AF pathogenesis.
- A comprehensive synthesis of immune mechanisms in AF across multiple domains was lacking.
Purpose of the Study:
- To systematically review and synthesize evidence on immune dysregulation in atrial fibrillation.
- To integrate findings from histological, mechanistic, prognostic, and genetic studies.
- To assess the role of immune factors in AF development, progression, and outcomes.
Main Methods:
- Systematic review of 16 studies (2009-2025) including histological, mechanistic, prognostic, and genetic analyses.
- Data extraction on immune cells, cytokines, signaling pathways, and clinical outcomes.
- Risk of bias and certainty of evidence assessment using ROBINS-I, RoB 2, and GRADE frameworks.
Main Results:
- Histological studies show T lymphocyte and macrophage infiltration in AF atria, linked to atrial dilatation and fibrosis.
- Epicardial adipose tissue harbors memory T cells promoting IL-17 and IFN-γ mediated inflammation.
- Mechanistic studies identify CD8+PAR1+ cytotoxic T cells, PD-1/PD-L1 disruption, and adipose-myocardial crosstalk as AF drivers.
- Immune biomarkers offer incremental prognostic value over conventional risk scores.
- Genetic evidence supports a causal role for immune dysregulation in AF susceptibility and progression.
Conclusions:
- Immune dysregulation is a primary determinant of atrial fibrillation development, progression, and outcomes.
- Immune biomarkers can enhance risk stratification for AF patients.
- Targeting immune pathways may lead to novel therapeutic strategies for AF.

