Key result
Serum IL-11 correlates with fibrosis markers in AF patients and its inhibition attenuates fibrosis in mice.
Why the study?
Inflammatory cytokines are closely associated with developing cardiac fibrosis, prompting exploration of the role of IL-11 in atrial fibrosis progression and potential therapeutic targeting.
Is IL-11 elevated in AF patients and does IL-11 inhibition prevent atrial fibrosis in a mouse model?
Case-Control (n=367)
Is IL-11 elevated in AF patients and does IL-11 inhibition prevent atrial fibrosis in a mouse model?
Effect estimate: r = 0.394
p-value: p=<0.001
IL-11 is elevated in AF patients and correlates with fibrosis markers, while its inhibition attenuates atrial fibrosis in preclinical models, suggesting a potential therapeutic target.
IL-11 correlates with AF fibrosis markers; observational data leave therapeutic targeting open pending trials.
INTRODUCTION: Inflammatory cytokines are closely associated with developing cardiac fibrosis. This research aimed to explore the significant role of IL-11 in atrial fibrosis progression and potential therapeutic targets. METHODS: 207 AF patients and 160 healthy subjects were included in the case-control study. Blood samples were analyzed for the level of IL-11 by enzyme-linked immunosorbent assay (ELISA). Angiotensin II (Ang II)-treated fibrosis mouse models were generated, and expression of IL-11 mRNA and protein was detected by RT-qPCR and Western blot. IL-11 antagonist was used to evaluating atrial fibrosis-related markers. RESULTS: The persistent atrial fibrillation patients (n = 76) had significantly larger left atrial size, higher serum levels of hypertrophic protein BNP, proinflammatory cytokine high-sensitivity C-reactive protein (hs-CRP), and interleukin-6 (IL-6) compared to paroxysmal atrial fibrillation patients (n = 131), and healthy subjects (all p < 0.05). Pearson correlation analysis revealed significant positive correlation between serum IL-11 and cardiac fibrosis markers BNP (r = 0.394, p < 0.001), CTX-I (r = 0.418, p < 0.001), PICP (r = 0.306, p < 0.001), PIIINP (r = 0.335, p < 0.001), and TGF-β1 (r = 0.273, p < 0.001). In the fibrosis mouse model, Ang II infusion significantly upregulated IL-11 mRNA and protein expression in the left atrium of mice (p < 0.05), as well as staining intensity of Masson trichrome, the intensity of α-SMA, and it increased mRNA expression of collagen I and III in atrial tissue. IL-11 antagonist treatment significantly attenuated Masson trichrome, number of α-SMA-positive myofibroblasts in atrial tissue. Also, it significantly reduced the p-ERK1/2 in atrial tissue of mice infused with Ang II (p < 0.05). CONCLUSIONS: IL-11 is upregulated in the serum of AF patients, and IL-11 inhibitor significantly inhibited Ang II-induced atrial fibrosis, a key pathological feature of AF. Therefore, IL-11 could be a potential therapeutic target for AF.
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Cong et al. (2023) conducted a case-control in Atrial Fibrillation (n=367). IL-11 vs. Healthy subjects was evaluated on Correlation between serum IL-11 and cardiac fibrosis marker BNP (r = 0.394, p=<0.001). Serum IL-11 levels were significantly correlated with cardiac fibrosis markers in AF patients (e.g., BNP r=0.394, p<0.001), and IL-11 inhibition attenuated atrial fibrosis in a mouse model.
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