Key result
PD-1 deficiency in C57BL/6 mice significantly increased inflammatory cytokines and intracellular reactive oxygen species, resulting in atrial electrical and structural remodeling.
Why the study?
Does PD-1 deficiency increase inflammatory cytokines, oxidative stress, and atrial remodeling in C57BL/6 mice?
Does PD-1 deficiency increase inflammatory cytokines, oxidative stress, and atrial remodeling in C57BL/6 mice?
Absolute Event Rate: 165.21% vs 35.47%
p-value: p=<0.001
PD-1 deficiency in mice leads to elevated systemic inflammation and oxidative stress, resulting in atrial electrical and structural remodeling that may increase susceptibility to atrial fibrillation.
Deficiency of the programmed cell death-1 (PD-1) gene enhances T-cell activation and increases inflammation levels. It has been reported that atrial fibrillation (AF) is closely related to inflammation. The aim of the present study was to investigate the role of PD-1 deficiency in the pathogenesis of AF. Two groups of mice were used in our experiment: the C57BL/6 and the C57BL/6-PD-(1-/-) group. The expression of the inflammatory cytokines interleukin (IL)-2, -4, -6, -10, -17, interferon-γ and tumor necrosis factor were detected. Furthermore, the levels of atrial myocyte oxidative stress, the atrial effective refractory period (AERP) and the atrial myocardial fibrosis levels were determined. Compared with the C57BL/6 group, we found that the inflammatory cytokines were significantly increased in the PD-1(-/-) group and the levels of atrial myocyte oxidative stress in the PD-1(-/-) group were also higher. The AERP became shorter and the dispersion of AERP was increased in the PD-1(-/-) group. Moreover, the PD-1(-/-) group presented significant atrial myocardial fibrosis but the C57BL/6 group did not. Our findings strongly suggest that the higher levels of inflammatory cytokines and atrial myocyte oxidative stress were present in the PD-1(-/-) mice and resulted in atrial electricity and structural remodeling. Due to the atrial remodeling, the PD-1(-/-) mice were more likely to develop AF.
No takes yet. Share an insight, caveat, or question.
Fu et al. (2012) studied Atrial remodeling and atrial fibrillation (n=30). PD-1 deficiency vs. Wild-type C57BL/6 mice was evaluated on Serum Interleukin-6 (IL-6) levels (pg/ml) (p=<0.001). PD-1 deficiency in C57BL/6 mice significantly increased inflammatory cytokines and intracellular reactive oxygen species, resulting in atrial electrical and structural remodeling.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: