Increased serum high mobility group box 1 protein in patients with atrial fibrillation

Hu, Xiaorong; Zhou, Wen‐Jie; Bai, Qijun; Wang, Jichun; Yang, Xiaoqin; Xu, Changwu; Lu, Zhibing; Xia, Hao; Jiang, Hong

doi:10.1016/j.biomag.2010.10.003

Cited by 16 publications

(24 citation statements)

References 23 publications

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“…Recently, Hu et al [8] also reported that the level of serum HMGB1 was significantly increased in patients with AF including paroxysmal and persistent AF. Meanwhile, the level of serum HMGB1 was positively correlated with the serum level of hs-CRP which was significantly increased in AF patients and was an important predictor for successful cardioversion and maintenance of sinus rhythm after conversion in AF patients [9].…”

mentioning

confidence: 94%

“…These results suggested that pro-inflammatory cytokines may play an important role in development and recurrence of AF and be a possible pathogenic link to AF. Recent studies revealed that HMGB1, a non-chromosomal nuclear protein, could regulate gene transcription and maintain the nucleosome structure and function as a novel pro-inflammatory cytokine in cardiovascular diseases [6][7][8].…”

mentioning

confidence: 99%

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Decreased serum endogenous secretory receptor for advanced glycation endproducts and increased cleaved receptor for advanced glycation endproducts levels in patients with atrial fibrillation

Zhao

Wang

2012

International Journal of Cardiology

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confidence: 94%

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confidence: 99%

Decreased serum endogenous secretory receptor for advanced glycation endproducts and increased cleaved receptor for advanced glycation endproducts levels in patients with atrial fibrillation

Zhao

Wang

2012

International Journal of Cardiology

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“…Myocardial ischemia and reperfusion (I/R) has been shown to induce local myocardial inflammation, the generation of reactive oxygen species (ROS) and apoptosis, which resulted in myocardial cell damage (3,4). Previous studies revealed that high mobility group box 1 (HMGB1) protein, a novel pro-inflammatory factor that is passively released from necrotic and apoptotic cells, or secreted by activated immune cells, serves an important role in the pathogenesis of inflammatory diseases, including acute hepatic necrosis, atrial fibrillation, myocardial infarction and myocardial I/R injury (5)(6)(7)(8). Furthermore, inhibition of HMGB1 has been demonstrated to attenuate myocardial I/R injury (5,8).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-451 protects against cardiomyocyte anoxia/reoxygenation injury by inhibiting high mobility group box 1 expression

Xie

et al. 2016

Molecular Medicine Reports

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High mobility group box 1 (HMGB1) protein serves an important role in myocardial ischemia/reperfusion (I/R) injury. MicroRNAs (miRNAs) are a group of small non‑coding RNAs that regulate numerous signaling pathways involved in myocardial I/R injury. The present study aimed to investigate whether miR‑451 protects against cardiomyocyte anoxia/reoxygenation (A/R) injury by attenuating HMGB1 expression. Neonatal rat ventricular cardiomyocytes were prepared and then subjected to A/R injury. The effect of upregulation or downregulation of miR‑451 on cell viability, apoptosis, superoxide dismutase (SOD) activity, and the expression of cleaved‑caspase‑3 and HMGB1 were measured accordingly. A luciferase assay was performed to further confirm whether miR‑451 can directly recognize the 3'‑untranslated region of HMGB1 in HEK293 cells. The expression of miR‑451 was significantly decreased in the cardiomyocytes during A/R, and upregulation of miR‑451 led to increased miR‑451 expression (P<0.05). Upregulation of miR‑451 significantly attenuated the loss of cardiomyocyte viability (P<0.05) and increased the intracellular levels of SOD during A/R (P<0.05). Furthermore, upregulation of miR‑451 significantly decreased the apoptosis of cardiomyocytes during A/R (P<0.05). The HMGB1 mRNA and protein expression levels were significantly downregulated in the Ad‑miR‑451 group compared with those in the A/R group (P<0.05). In addition, upregulation of miR‑451 reduced its translocation from the nucleus to the cytoplasm. The luciferase assay confirmed that HMGB1 mRNA is a direct target of miR‑451 in cardiomyocytes. In conclusion, the present study suggested that upregulation of miR‑451 could protect against A/R‑induced cardiomyocyte injury by inhibiting HMGB1 expression.

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“…HMGB1 has been demonstrated to be a pro-inflammatory cytokine in certain cardiovascular diseases (3–6). A previous study showed that HMGB1 acts as an early mediator of inflammation during myocardial ischemia-reperfusion (I/R) as well as classical early pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), and may promote the release of TNF-α and IL-6.…”

Section: Introductionmentioning

confidence: 99%

Postconditioning with rosuvastatin reduces myocardial ischemia-reperfusion injury by inhibiting high mobility group box 1 protein expression

Wei

2013

Experimental and Therapeutic Medicine

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High mobility group box 1 protein (HMGB1) plays an important role in myocardial ischemia-reperfusion (I/R) injury. Rosuvastatin (RS) preconditioning has been reported to reduce myocardial I/R injury. The aim of this study was to investigate whether postconditioning with RS is able to reduce myocardial I/R injury by inhibiting HMGB1 expression in rats. Anesthetized male rats were subjected to ischemia for 30 min and treated once with RS (10 mg/kg, i.v.) 5 min prior to reperfusion for 4 h. Lactate dehydrogenase (LDH), creatine kinase (CK) and superoxide dismutase (SOD) activities, malondialdehyde (MDA) levels and infarct size were measured. HMGB1 expression was assessed by immunoblotting. The results showed that RS postconditioning significantly decreased the infarct size and the activities of LDH and CK following 4 h reperfusion (all P<0.05). RS postconditioning also significantly inhibited the increase of MDA levels and the reduction of SOD activity (both P<0.05). RS postconditioning was able to significantly inhibit the HMGB1 expression induced by I/R. The present study suggested that postconditioning with RS reduces myocardial I/R injury, which may be associated with the inhibition of HMGB1 expression.

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Increased serum high mobility group box 1 protein in patients with atrial fibrillation

Cited by 16 publications

References 23 publications

Decreased serum endogenous secretory receptor for advanced glycation endproducts and increased cleaved receptor for advanced glycation endproducts levels in patients with atrial fibrillation

Decreased serum endogenous secretory receptor for advanced glycation endproducts and increased cleaved receptor for advanced glycation endproducts levels in patients with atrial fibrillation

MicroRNA-451 protects against cardiomyocyte anoxia/reoxygenation injury by inhibiting high mobility group box 1 expression

Postconditioning with rosuvastatin reduces myocardial ischemia-reperfusion injury by inhibiting high mobility group box 1 protein expression

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