High mobility group box 1 protein： possible pathogenic link to atrial fibrillation  

作　　者：HU Xiao-rong WANG Xiao-hong LIU Hua-fen ZHOU Wen-jie JIANG Hong 

机构地区：[1]Department of Cardiology,Renmin Hospital of Wuhan University,Cardiovascular Research Institute of Wuhan University,Wuhan,Hubei 430060,China

出　　处：《Chinese Medical Journal》2012年第13期2346-2348,共3页中华医学杂志（英文版）

基　　金：This study was partly supported by a grant from National Natural Science Foundation of China （No. 81070143）. The authors declare that they have no conflict of interest.

摘　　要：Atrial fibrillation （AF） is the most common sustained dysrhythmia in clinical practice. The bulk of evidence suggests that inflammatory processes, oxidative stress and matrix metalloproteinase are associated with development of AF. However, these agents may be involved in high mobility group box 1 protein （HMGB1）. We hypothesized that HMGB1 may be a possible pathogenic link to AF. A growing body of evidence supports these hypotheses. First, the level of serum HMGB1 is significantly increased in patients with AF including paroxysmal and persistent AF. Second, HMGB1 has been identified as a new pro-inflammatory cytokine in cardiovascular diseases, along with tumor necrosis factor （TNF）-a, interleukin （IL）-6, and C-reactive protein, and there is cross-talk between HMGB1 and inflammatory cytokines. Third, oxidative stress is involved in the release of the pro-inflammatory cytokine, HMGB1, indicating there is cross-talk between oxidative stress and inflammation, and oxidative stress may reinforce the effect of inflammation on the pathogenesis of AF and inflammation may play a more important role in the pathogenesis of AF. Fourth, HMGB1 can promote matrix metalloproteinase-9 upregulation and activation. Fifth, HMGB1 receptors （receptor for advanced glycation end products, Toll-like receptor-2,4） may mediate the atrial structural remodeling or be up-regulated in patients with non-valvular AF. These results suggest that HMGB1 may participate in the pathogenesis of AF and provide a potential target for pharmacoloclical interruption of AF.Atrial fibrillation （AF） is the most common sustained dysrhythmia in clinical practice. The bulk of evidence suggests that inflammatory processes, oxidative stress and matrix metalloproteinase are associated with development of AF. However, these agents may be involved in high mobility group box 1 protein （HMGB1）. We hypothesized that HMGB1 may be a possible pathogenic link to AF. A growing body of evidence supports these hypotheses. First, the level of serum HMGB1 is significantly increased in patients with AF including paroxysmal and persistent AF. Second, HMGB1 has been identified as a new pro-inflammatory cytokine in cardiovascular diseases, along with tumor necrosis factor （TNF）-a, interleukin （IL）-6, and C-reactive protein, and there is cross-talk between HMGB1 and inflammatory cytokines. Third, oxidative stress is involved in the release of the pro-inflammatory cytokine, HMGB1, indicating there is cross-talk between oxidative stress and inflammation, and oxidative stress may reinforce the effect of inflammation on the pathogenesis of AF and inflammation may play a more important role in the pathogenesis of AF. Fourth, HMGB1 can promote matrix metalloproteinase-9 upregulation and activation. Fifth, HMGB1 receptors （receptor for advanced glycation end products, Toll-like receptor-2,4） may mediate the atrial structural remodeling or be up-regulated in patients with non-valvular AF. These results suggest that HMGB1 may participate in the pathogenesis of AF and provide a potential target for pharmacoloclical interruption of AF.

关 键 词：atrial fibrillation high mobility group box l protein INFLAMMATION oxidative stress matrix metalloproteinase 

分 类 号：Q55[生物学—生物化学] TN386.1[电子电信—物理电子学]