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May 21, 2020Experimental and Therapeutic MedicineOpen Access

Interleukin‑22 is elevated in the atrium and plasma of patients with atrial fibrillation and increases collagen synthesis in transforming growth factor‑β1‑treated cardiac fibroblasts via the JNK pathway

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Why the study?

IL-22 is involved in cardiovascular diseases such as hypertension, cardiac fibrosis, and aortic dissection, but its expression in patients with AF was unknown.

Population

Patients with AF (paroxysmal, persistent, permanent) and donors with sinus rhythm or without AF history

Comparison

Patients with AF vs donors with sinus rhythm or without AF history, plus in vitro fibroblast assays

Design

Translational case-control and in vitro laboratory study

Authors

YWYongxin WuSun Yat-sen UniversityLTLihua TanTianjin University of Traditional Chinese MedicineLSLei ShiSoochow University

Discussion

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Member takes

Overview

IL-22 expression in AF atria may reflect local inflammation; leaves open mechanistic role and therapeutic targeting pending prospective validation.

Structured PICO

P
Population
56 patients with valvular and rheumatic heart disease undergoing heart valve replacement (35 with permanent AF, 21 with sinus rhythm) for atrial tissue analysis, and 195 patients (155 with AF, 40 non-AF controls) for blood sample analysis. In vitro studies used primary mouse cardiac fibroblasts.
I
Intervention
In vitro treatment with recombinant mouse IL-22 (10 ng/ml) added to TGF-β1 (10 ng/ml) for 12 hours.
C
Comparator
In vitro treatment with vehicle, TGF-β1 alone, or TGF-β1 + IL-22 + JNK inhibitor SP600125 (30 µM).
O
Outcome
IL-22 expression levels in atrial tissue and plasma, and in vitro expression of α-SMA, collagen I, and collagen III in cardiac fibroblasts.surrogate

IL-22 is upregulated in atrial fibrillation and may promote atrial fibrosis by enhancing TGF-β1-induced collagen synthesis through the JNK pathway, suggesting a potential therapeutic target.

Limitations

  • Animal studies still need to be performed to confirm this hypothesis

Cite This Study

Wu et al. (2020) studied this question.

synapsesocial.com/papers/6a7280c75d37378ac1df424chttps://doi.org/10.3892/etm.2020.8778
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Increased Expressions of IL-22 and Th22 cells in the coxsackievirus B3-Induced mice acute viral myocarditis2012 · 39 citations
  2. 2Temporal Relations of Atrial Fibrillation and Congestive Heart Failure and Their Joint Influence on Mortality2003 · 1,988 citations
  3. 3Upregulation of sestrins protect atriums against oxidative damage and fibrosis in human and experimental atrial fibrillation2017 · 31 citations
  4. 4IL-22 exacerbates the severity of CVB3-induced acute viral myocarditis in IL-17A-deficient mice2013 · 21 citations
  5. 5Interleukin-22 is increased in multiple sclerosis patients and targets astrocytes2015 · 110 citations