Omentin-1 is associated with atrial fibrillation in patients with cardiac valve disease

Chen, Yubin; Liu, Fen; Han, Fei; Lv, Li-Zhi; Tang, Cui; Xie, Zhongshang; Luo, Fanyan

doi:10.1186/s12872-020-01478-1

Cited by 18 publications

(15 citation statements)

References 35 publications

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“…In addition, omentin-1 suppresses the JAK-2/STAT3 pathway activation, contributing to its anti-inflammatory role and ameliorating MMP expression [84]. Interestingly, omentin-1 concentration was found to be decreased in response to hypoxia [85], in line with current results which showed a negative correlation between omentin and HIF-1α levels, indicating that hypoxia could be the early trigger for altering omentin secretion. Decreased omentin-1 levels can lead to enhanced VEGF expression, and consequently cell migration and angiogenesis [86], in addition to increased resistance to apoptosis through decreased bax/bcl-2 protein ratio [87].…”

Section: Discussionsupporting

confidence: 85%

Association of the Adipokines Chemerin, Apelin, Vaspin and Omentin and Their Functional Genetic Variants with Rheumatoid Arthritis

Wahba

Ibrahim

Abo-Elmatty

et al. 2021

JPM

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Adipokines were shown to exert crucial roles in rheumatic diseases. This study aimed to assess the role of chemerin, apelin, vaspin, and omentin adipokines and their genetic variants rs17173608, rs2235306, rs2236242, and rs2274907, respectively, in rheumatoid arthritis (RA) pathogenesis in Egyptian patients. A total of 150 RA patients and 150 healthy individuals were recruited. Blood samples were collected and used for genotyping. Serum was separated and used for expression analysis by quantitative PCR, and various biochemical markers determination by ELISA. Serum protein levels of chemerin and vaspin, as well as their gene expression levels were higher, while those of apelin and omentin were lower in RA patients and were associated with most of RA clinical and laboratory characteristics. G allele of chemerin rs17173608, T allele of vaspin rs2236242, and T allele of omentin rs2274907 were more frequent in RA patients. Serum levels and gene expression levels of chemerin in GG genotype carriers and vaspin in TT genotype group were significantly higher, while those of omentin in TT genotype carriers were significantly lower than RA patients with other genotypes. There was no association between apelin rs2235306 and RA. Chemerin rs17173608, vaspin rs2236242, and omentin rs2274907 polymorphisms were associated with increased susceptibility to RA.

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Section: Discussionsupporting

confidence: 85%

Association of the Adipokines Chemerin, Apelin, Vaspin and Omentin and Their Functional Genetic Variants with Rheumatoid Arthritis

Wahba

Ibrahim

Abo-Elmatty

et al. 2021

JPM

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“…Images of cells were taken at x100 magnification after 0, 24 and 48 h (Olympus Corporation). The wound closure rate [(initial wound area-wound area at 24 h)/initial wound area] was analyzed using Image Pro Plus 6.0 software (Media Cybernetics, Inc.) (18).…”

Section: -Ethynyl-2'-deoxyuridine (Edu) Labeling Assay 5-8fmentioning

confidence: 99%

Galectin‑3 facilitates the proliferation and migration of nasopharyngeal carcinoma cells via activation of the ERK1/2 and Akt signaling pathways, and is positively correlated with the inflammatory state of nasopharyngeal carcinoma

Chen

Liu

et al. 2021

Mol Med Rep

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Nasopharyngeal carcinoma (NPC) is an epithelial carcinoma originating from the nasopharyngeal mucosal tissue and is highly prevalent in southeast Asia. Galectin-3 (gal-3) serves crucial roles in many cancers but its role in NPC remains to be elucidated. The aim of the present study was to investigate the role of gal-3 in NPC. Immunohistochemistry and ELISA were used to determine the expression level of gal-3 in patients with NPC or chronic rhinitis (CR). Gal-3 short hairpin (sh)RNA was established to knockdown gal-3 in 5-8F and 6-10B cells, allowing for the evaluation of the roles of gal-3 in proliferation, migration and apoptosis in NPC cell lines. Immunohistochemistry staining of IL-6 and IL-8 was applied to access the inflammatory state of tumor tissues, and the correlation between the inflammatory state and gal-3 was analyzed. The results demonstrated that gal-3 was upregulated in patients with NPC compared with patients with CR. Knockdown of gal-3 inhibited proliferation and migration in 5-8F and 6-10B cells, as well as promoted apoptosis in these cells. The expression levels of MMP-9 and IL-8 were also decreased in 5-8F and 6-10B cells after transfection with gal-3 shRNA. A positive correlation was identified between the expression level of gal-3 and the inflammatory state of NPC. The phosphorylation levels of ERK1/2 and Akt were downregulated after knockdown of gal-3 in 5-8F and 6-10B cells. In conclusion, the expression level of gal-3 was upregulated in patients with NPC and was positively correlated with the inflammatory state of NPC. The results suggested that gal-3 promoted the proliferation and migration of 5-8F and 6-10B cells, while inhibiting the apoptosis of these cells. Moreover, activation of ERK1/2 and Akt may be the underlying mechanism of the effects of gal-3 on NPC.

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“…EAT-mediated atrial fibrosis has been linked to the PeAF subtype, and CD8 + lymphocyte infiltrates are seemingly involved [ 76 ]. Angiopoietin-like protein 2 (Angptl2), YKL-40, CTGF, activin A (TGF-β superfamily) upregulation and Omentin-1 downregulation in human EAT are also implicated in atrial fibrosis and AF development [ 60 , 77 , 78 , 79 , 80 ].…”

Section: Atrial Fibrillation Pathogenesismentioning

confidence: 99%

Molecular Insights in Atrial Fibrillation Pathogenesis and Therapeutics: A Narrative Review

et al. 2021

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The prevalence of atrial fibrillation (AF) is bound to increase globally in the following years, affecting the quality of life of millions of people, increasing mortality and morbidity, and beleaguering health care systems. Increasingly effective therapeutic options against AF are the constantly evolving electroanatomic substrate mapping systems of the left atrium (LA) and ablation catheter technologies. Yet, a prerequisite for better long-term success rates is the understanding of AF pathogenesis and maintenance. LA electrical and anatomical remodeling remains in the epicenter of current research for novel diagnostic and treatment modalities. On a molecular level, electrical remodeling lies on impaired calcium handling, enhanced inwardly rectifying potassium currents, and gap junction perturbations. In addition, a wide array of profibrotic stimuli activates fibroblast to an increased extracellular matrix turnover via various intermediaries. Concomitant dysregulation of the autonomic nervous system and the humoral function of increased epicardial adipose tissue (EAT) are established mediators in the pathophysiology of AF. Local atrial lymphomononuclear cells infiltrate and increased inflammasome activity accelerate and perpetuate arrhythmia substrate. Finally, impaired intracellular protein metabolism, excessive oxidative stress, and mitochondrial dysfunction deplete atrial cardiomyocyte ATP and promote arrhythmogenesis. These overlapping cellular and molecular alterations hinder us from distinguishing the cause from the effect in AF pathogenesis. Yet, a plethora of therapeutic modalities target these molecular perturbations and hold promise in combating the AF burden. Namely, atrial selective ion channel inhibitors, AF gene therapy, anti-fibrotic agents, AF drug repurposing, immunomodulators, and indirect cardiac neuromodulation are discussed here.

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Omentin-1 is associated with atrial fibrillation in patients with cardiac valve disease

Cited by 18 publications

References 35 publications

Association of the Adipokines Chemerin, Apelin, Vaspin and Omentin and Their Functional Genetic Variants with Rheumatoid Arthritis

Association of the Adipokines Chemerin, Apelin, Vaspin and Omentin and Their Functional Genetic Variants with Rheumatoid Arthritis

Galectin‑3 facilitates the proliferation and migration of nasopharyngeal carcinoma cells via activation of the ERK1/2 and Akt signaling pathways, and is positively correlated with the inflammatory state of nasopharyngeal carcinoma

Molecular Insights in Atrial Fibrillation Pathogenesis and Therapeutics: A Narrative Review

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