Proteína C reactiva y fibrilación auricular. Un viejo marcador en busca de un nuevo sitio

Madrid, Antonio Hernández

doi:10.1157/13084635

Cited by 8 publications

(3 citation statements)

References 20 publications

(21 reference statements)

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“…CRP is one of the most commonly used markers for inflammation. Recently, an increasing body of evidence showed strong association between inflammation and the pathogenesis of AF [3,8,9,27]. Therefore, elevated CRP level is used as a prognostic marker for AF [9].…”

Section: Discussionmentioning

confidence: 99%

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C-reactive protein promotes inflammation through TLR4/NF-κB/TGF-β pathway in HL-1 cells

Sun

Gao

et al. 2019

Bioscience Reports

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Atrial fibrillation (AF) is the most common type of heart arrhythmia. Currently, the pathogenesis of AF is not fully understood yet. A growing body of evidence highlighted the strong association between inflammation and the pathogenesis of AF. C-reactive protein (CRP) is an inflammation marker with increased expression in AF. Therefore, the aim of this study was to determine if CRP promotes inflammation, which may sequentially mediate the onset of AF and the concurrent atrial fibrosis, through TLR4/NF-κB/TGF-β pathway. HL-1 cells were treated with either 25 or 50 μg/ml recombinant human CRP. TGF-β1 and NF-κB inhibitors were given either solely or together to the 50 μg/ml CRP-treated cells. Cell proliferation, apoptosis, the expression of apoptotic factors and TLR4, IL-6, TGF-β1, Smad2, and the phosphorylation of Smad2 were determined. Data showed that CRP induced dose-dependent inhibition on cell proliferation and promoted cell apoptosis, which was induced through both intrinsic and extrinsic pathways. Such effects were reversed by inhibiting TGF-β1 and/or NF-κB. Inhibition of TGF-β1 and/or NF-κB also reduced the expression of TLR4 and IL-6. Inhibition of NF-κB alone weakened the expression of TGF-β1 and phosphorylation of Smad2. Our study demonstrated that CRP is not only a marker, but also an important mediator in the induction of inflammation and likely the pathogenesis of AF. We for the first time reported CRP-induced activation and cross-talk between TLR4 and NF-κB/TGF-β1 signaling pathway in a cardiomyocyte model. Reducing CRP and targeting TLR4/NF-κB/TGF-β1 pathway may provide new insights in the therapeutic interventions to inflammation-induced AF.

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Section: Discussionmentioning

confidence: 99%

“…Recently, an increasing body of evidence showed strong association between inflammation and the pathogenesis of AF [3,8,9,27]. Therefore, elevated CRP level is used as a prognostic marker for AF [9]. However, except for being a marker for AF, CRP per se is also found to trigger inflammation [13].…”

Section: Discussionmentioning

confidence: 99%

C-reactive protein promotes inflammation through TLR4/NF-κB/TGF-β pathway in HL-1 cells

Sun

Gao

et al. 2019

Bioscience Reports

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“…Changes in inflammation are common in the tumor therapy-induced AF (Aviles et al, 2003 ; Siemes et al, 2006 ; Erichsen et al, 2012 ). Inflammation, determined by elevations of the concentrations of related biomarkers, is associated with the presence or development of AF (Hernández, 2006 ). Furthermore, cancer-related systemic inflammation promotes and maintains AF by inducing atrial structural remodeling, such as that in tumor necrosis factor (TNF)-α, nuclear factor (NF)-κB, and macrophage migration inhibitory factor (MIF) (Guzzetti et al, 2002 ).…”

Section: Mechanisms Of Anticancer Drug-induced Afmentioning

confidence: 99%

Anticancer Therapy-Induced Atrial Fibrillation: Electrophysiology and Related Mechanisms

Yang

Yuan

et al. 2018

Front. Pharmacol.

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Some well-established immunotherapy, radiotherapy, postoperation, anticancer drugs such as anthracyclines, antimetabolites, human epidermal growth factor receptor 2 blockers, tyrosine kinase inhibitors, alkylating agents, checkpoint inhibitors, and angiogenesis inhibitors, are significantly linked to cardiotoxicity. Cardiotoxicity is a common complication of several cancer treatments. Some studies observed complications of cardiac arrhythmia associated with the treatment of cancer, including atrial fibrillation (AF), supraventricular arrhythmias, and cardiac repolarization abnormalities. AF increases the risk of cardiovascular morbidity and mortality; it is associated with an almost doubled risk of mortality and a nearly 5-fold increase in the risk of stroke. The occurrence of AF is also usually researched in patients with advanced cancer and those undergoing active cancer treatments. During cancer treatments, the incidence rate of AF affects the prognosis of tumor treatment and challenges the treatment strategy. The present article is mainly focused on the cardiotoxicity of cancer treatments. In our review, we discuss these anticancer therapies and how they induce AF and consequently provide information on the precaution of AF during cancer treatment.

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Cardiovascular Disease

Fernandes¹,

Providência²,

Reis³

et al. 2015

Biomarkers of Cardiometabolic Risk, Inflammation and Disease

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Proteína C reactiva y fibrilación auricular. Un viejo marcador en busca de un nuevo sitio

Cited by 8 publications

References 20 publications

C-reactive protein promotes inflammation through TLR4/NF-κB/TGF-β pathway in HL-1 cells

C-reactive protein promotes inflammation through TLR4/NF-κB/TGF-β pathway in HL-1 cells

Anticancer Therapy-Induced Atrial Fibrillation: Electrophysiology and Related Mechanisms

Cardiovascular Disease

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