T helpers 17 cell responses induced cardiac hypertrophy and remodeling in essential hypertension

Xu, Liang; Chen, Guanghua; Liang, Yi; Zhou, Cuicui; Zhang, Fen; Fan, Tingpan; Chen, Xinxin; Zhou, Hong; Yuan, Wei

doi:10.20452/pamw.15811

Cited by 7 publications

(10 citation statements)

References 17 publications

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“…Th17 cell differentiation was enriched in subgroup III, in which BMI was significantly higher than that in the other subgroups, suggesting that Th17 cell differentiation is related with the clinical characteristics of BMI. Moreover, Th17 cell differentiation is involved in many inflammatory cardiovascular diseases and plays a critical role in the pathogenesis of myocardial dysfunction, 21) which is consistent with the clinical characteristics of subgroup III.…”

Section: Discussionsupporting

confidence: 62%

Subgroup Identification with Gene Expression Profiles of Adipose Tissue in Patients with Coronary Artery Disease

et al. 2021

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Section: Discussionsupporting

confidence: 62%

Subgroup Identification with Gene Expression Profiles of Adipose Tissue in Patients with Coronary Artery Disease

et al. 2021

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“…22 In 187 hypertensive adults and 70 healthy controls, an increased percentage of Th17 was observed in hypertensive patients, particularly in adults with left ventricular (LV) hypertrophy. 24 Th17 is associated with the progression of NAFLD from NAFL to NASH to liver fibrosis. 25 Previous studies have shown that the liver microenvironment increases macrophage infiltration and hepatocyte balloon-like degeneration by changing the features of the liver Th17 cells, and the mechanism is related to the activation of the C-X-C motif chemokine receptor (CXCR)3/C-X-C motif chemokine ligand (CXCL)9/10 axis.…”

Section: Discussionmentioning

confidence: 99%

“…A study involving 77 patients with HF showed an increase in the IL‐17 plasma level, which was negatively correlated with LVEF and fractional shortening 22 . In 187 hypertensive adults and 70 healthy controls, an increased percentage of Th17 was observed in hypertensive patients, particularly in adults with left ventricular (LV) hypertrophy 24 . Th17 is associated with the progression of NAFLD from NAFL to NASH to liver fibrosis 25 .…”

Section: Discussionmentioning

confidence: 99%

Heart failure with preserved ejection fraction and non‐alcoholic fatty liver disease: new insights from bioinformatics

Wang

Li²,

Sun³

et al. 2022

ESC Heart Failure

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Aims Heart failure with preserved ejection fraction (HFpEF) and non‐alcoholic fatty liver disease (NAFLD) are related conditions with an increasing incidence. The mechanism of their relationship remains undefined. Here, we aimed to explore the potential mechanisms, diagnostic markers, and therapeutic options for HFpEF and NAFLD. Methods and results HFpEF and NAFLD datasets were downloaded from the Gene Expression Omnibus (GEO) database. Common differentially expressed genes (DEGs) were screened for functional annotation. A protein–protein interaction network was constructed based on the STRING database, and hub genes were analysed using GeneMANIA annotation. ImmuCellAI (Immune Cell Abundance Identifier) was employed for analysis of immune infiltration. We also used validation datasets to validate the expression levels of hub genes and the correlation of immune cells. To screen for diagnostic biomarkers, we employed the least absolute shrinkage and selection operator and support vector machine‐recursive feature elimination. Drug signature database was used to predict potential therapeutic drugs. Our analyses identified a total of 33 DEGs. Inflammation and immune infiltration played important roles in the development of both diseases. The data showed a close relationship between chemokine signalling pathway, cytokine–cytokine receptor interaction, calcium signalling pathway, neuroactive ligand–receptor interaction, osteoclast differentiation, and cyclic guanosine monophosphate‐protein kinase G signalling pathway. We demonstrated that PRF1 (perforin 1) and IL2RB (interleukin‐2 receptor subunit beta) proteins were perturbed by the diseases and may be the hub genes. The analysis showed that miR‐375 may be a potential diagnostic marker for both diseases. Our drug prediction analysis showed that bosentan, eldecalcitol, ramipril, and probucol could be potential therapeutic options for the diseases. Conclusions Our findings revealed common pathogenesis, diagnostic markers, and therapeutic agents for HFpEF and NAFLD. There is need for further experimental studies to validate our findings.

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“…There is increasing interest in the use of markers and risk scores as well as in testing their clinical applicability in cardiovascular medicine [25][26][27][28][29][30][31][32][33]. Several factors have been found to be associated with LVH assessed by different modalities [7,16]. Studies performed so far have demonstrated that there is a relationship between CTR and LVM measured by echocardiography [5,34,35].…”

Section: Discussionmentioning

confidence: 99%

“…Increased LV mass (LVM) may arise from multiple molecular mechanism, is associated with adverse clinical outcomes and may implicate clinical decision-making [6,7]. CMR imaging is considered the gold standard for assessment of LVM [8].…”

Section: Introductionmentioning

confidence: 99%

Clinical Data, Chest Radiograph and Electrocardiography in the Screening for Left Ventricular Hypertrophy: The CAR2E2 Score

Matusik¹,

Bryll

Pac

et al. 2022

JCM

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Left ventricular hypertrophy (LVH) is associated with adverse clinical outcomes and implicates clinical decision-making. The aim of our study was to assess the importance of different approaches in the screening for LVH. We included patients who underwent cardiac magnetic resonance (CMR) imaging and had available chest radiograph in medical documentation. Cardiothoracic ratio (CTR), transverse cardiac diameter (TCD), clinical and selected electrocardiographic (ECG)-LVH data, including the Peguero-Lo Presti criterion, were assessed. CMR–LVH was defined based on indexed left ventricular mass-to-body surface area. Receiver operating characteristics analyses showed that both the CTR and TCD (CTR: area under the curve: [AUC] = 0.857, p < 0.001; TCD: AUC = 0.788, p = 0.001) were predictors for CMR–LVH. However, analyses have shown that diagnoses made with TCD, but not CTR, were consistent with CMR–LVH. From the analyzed ECG–LVH criteria, the Peguero-Lo Presti criterion was the best predictor of LVH. The best sensitivity for screening for LVH was observed when the presence of heart failure, ≥40 years in age (each is assigned 1 point), increased TCD and positive Peguero-Lo Presti criterion (each is assigned 2 points) were combined (CAR2E2 score ≥ 3 points). CAR2E2 score may improve prediction of LVH compared to other approaches. Therefore, it may be useful in the screening for LVH in everyday clinical practice in patients with prevalent cardiovascular diseases.

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T helpers 17 cell responses induced cardiac hypertrophy and remodeling in essential hypertension

Cited by 7 publications

References 17 publications

Subgroup Identification with Gene Expression Profiles of Adipose Tissue in Patients with Coronary Artery Disease

Subgroup Identification with Gene Expression Profiles of Adipose Tissue in Patients with Coronary Artery Disease

Heart failure with preserved ejection fraction and non‐alcoholic fatty liver disease: new insights from bioinformatics

Clinical Data, Chest Radiograph and Electrocardiography in the Screening for Left Ventricular Hypertrophy: The CAR2E2 Score

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