Assessment of heat shock proteins and endothelial dysfunction in acute pulmonary embolism

İn, Erdal; Deveci, Figen; Kaman, Dilara

doi:10.1097/mbc.0000000000000456

Cited by 6 publications

(3 citation statements)

References 33 publications

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“…The required induction of end-othelial dysfunction may be the result of the younger age of our animals because endothelial NO-production decreases with age (Liu et al 1992;Parker et al 2000). Also in humans, endothelial dysfunction is often present both in patients with acute pulmonary embolism, as well as with CTEPH, and correlates with disease severity (Reesink et al 2006;In et al 2016;Chibana et al 2017). In humans, CTEPH prevalence is higher in females (Kirson et al 2011), although male patients typically have a worse prognosis (Chen et al 2018).…”

Section: Animal Modelmentioning

confidence: 99%

Cardiac remodelling in a swine model of chronic thromboembolic pulmonary hypertension: comparison of right vs. left ventricle

Stam

Cai

Velde

et al. 2019

The Journal of Physiology

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Key points Right ventricle (RV) function is the most important determinant of survival and quality of life in patients with chronic thromboembolic pulmonary hypertension (CTEPH).The changes in right and left ventricle gene expression that contribute to ventricular remodelling are incompletely investigated.RV remodelling in our CTEPH swine model is associated with increased expression of the genes involved in inflammation (TGFβ), oxidative stress (ROCK2, NOX1 and NOX4), and apoptosis (BCL2 and caspase‐3).Alterations in ROCK2 expression correlated inversely with RV contractile reserve during exercise.Since ROCK2 has been shown to be involved in hypertrophy, oxidative stress, fibrosis and endothelial dysfunction, ROCK2 inhibition may present a viable therapeutic target in CTEPH. AbstractRight ventricle (RV) function is the most important determinant of survival and quality of life in patients with chronic thromboembolic pulmonary hypertension (CTEPH). The present study investigated whether the increased cardiac afterload is associated with (i) cardiac remodelling and hypertrophic signalling; (ii) changes in angiogenic factors and capillary density; and (iii) inflammatory changes associated with oxidative stress and interstitial fibrosis. CTEPH was induced in eight chronically instrumented swine by chronic nitric oxide synthase inhibition and up to five weekly pulmonary embolizations. Nine healthy swine served as a control. After 9 weeks, RV function was assessed by single beat analysis of RV–pulmonary artery (PA) coupling at rest and during exercise, as well as by cardiac magnetic resonance imaging. Subsequently, the heart was excised and RV and left ventricle (LV) tissues were processed for molecular and histological analyses. Swine with CTEPH exhibited significant RV hypertrophy in response to the elevated PA pressure. RV–PA coupling was significantly reduced, correlated inversely with pulmonary vascular resistance and did not increase during exercise in CTEPH swine. Expression of genes associated with hypertrophy (BNP), inflammation (TGFβ), oxidative stress (ROCK2, NOX1 and NOX4), apoptosis (BCL2 and caspase‐3) and angiogenesis (VEGFA) were increased in the RV of CTEPH swine and correlated inversely with RV–PA coupling during exercise. In the LV, only significant changes in ROCK2 gene‐expression occurred. In conclusion, RV remodelling in our CTEPH swine model is associated with increased expression of genes involved in inflammation and oxidative stress, suggesting that these processes contribute to RV remodelling and dysfunction in CTEPH and hence represent potential therapeutic targets.

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Section: Animal Modelmentioning

confidence: 99%

Cardiac remodelling in a swine model of chronic thromboembolic pulmonary hypertension: comparison of right vs. left ventricle

Stam

Cai

Velde

et al. 2019

The Journal of Physiology

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“…In the microvasculopathy observed in chronic thromboembolic pulmonary hypertension, pulmonary endothelium cells are known to play a key role, and it has a significant role both in the disease's development and in the targeted treatment . In recent years, pulmonary endothelial dysfunction in acute PTE has gradually become a point of focus, and various studies have reported increasing endothelial dysfunction markers in these groups of patients . According to our review, there is only one study investigating the serum endocan levels in patients with PTE in the literature.…”

Section: Discussionmentioning

confidence: 95%

Endocan as a marker of disease severity in pulmonary thromboembolism

Kuluöztürk

İn

İlhan

2019

Clinical Respiratory J

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Introduction The aim of this study is to determine the serum endocan levels in patients with pulmonary thromboembolism (PTE) and investigate whether a relationship exists between serum endocan levels and the disease severity. Materials and Methods The study included 85 patients with acute PTE and 40 healthy control subjects. The patients with PTE were divided into three groups at admission as “high‐risk”, “intermediate‐risk” and “low‐risk”, considering the guidelines of the European Society of Cardiology. Serum endocan levels in all participants' blood samples were measured. Results The mean serum endocan levels were significantly higher in the PTE group, compared to the control subjects (P < 0.001). Serum endocan levels were significantly higher in the “high‐risk” group when compared with patients in the “low‐risk” and “intermediate‐risk” groups (P < 0.001 and P < 0.01 respectively). Similarly, serum endocan levels were higher in the “intermediate‐risk” group compared to those in the “low‐risk” group (P < 0.001). There was a negative correlation between serum endocan levels and partial oxygen pressure (r = −0.262, P = 0.016), whereas a positive correlation was found between the serum endocan levels and systolic pulmonary arterial pressure (r = 0.296, P = 0.006). Additionally, endocan had an area under the curve in the receiver operating characteristic curve of 0.837 (0.768‐0.907; 95% CI; P < 0.001) and cut‐off value was 194.5 pg/mL (sensitivity 80%, specificity 72.5%). Conclusion Serum endocan levels were higher and related to the severity of the disease in PTE patients. Additionally, endocan could be an indicator to be used in the diagnosis of PTE and in the prediction of the disease severity.

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“…Prospective studies involving gene expression profiling in larger patient cohorts, functional validations, evaluation in real-world settings, and comparison with current methods are warranted before biomarkers can be confidently applied in clinical practice. [12,13] Methods:…”

Section: Introductionmentioning

confidence: 99%

Predicting biomarker for the acute pulmonary embolism by using gene ontology and machine learning

Zhou,

Duan,

Chen

et al. 2023

Preprint

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Key PointsEarly and Accurate Diagnosis Essential:Acute pulmonary embolism (PE) is a critical condition that demands prompt and precise diagnosis for effective treatment.Limitations of Current Diagnostics:Existing diagnostic methods like Computed Tomography Pulmonary Angiography (CTPA) have certain limitations, leading to the exploration of alternative approaches.Potential of Blood-Based Biomarkers:A recent study focused on identifying blood-based biomarkers for PE. This involved using gene ontology analysis and machine learning methods to analyze gene expression data from both PE patients and healthy controls.Gene Selection and Analysis:The study selected 20 genes for detailed analysis. These included various coagulation factors, fibrinolytic genes, and inflammation markers. Gene Ontology enrichment analysis was performed to understand the biological processes and molecular functions of these genes.Machine Learning for Diagnosis:Supervised machine learning algorithms were utilized to create classification models using the expression levels of these 20 genes. The models demonstrated promising results in distinguishing PE patients from healthy individuals.Acute pulmonary embolism (PE) is a life-threatening condition requiring early and accurate diagnosis. Current diagnostic methods like CTPA have limitations, and a study aimed to identify potential blood-based biomarkers for PE using gene ontology analysis and machine learning methods. Gene expression data of PE patients and healthy controls were obtained from the Gene Expression Omnibus database. A total of 20 genes were selected for further analysis, including coagulation factors F7, F10, F12, fibrinolytic genes PLAT, SERPINE1 and SERPINE2, and inflammation markers SELE, VCAM1 and ICAM. Gene Ontology enrichment analysis was performed to identify biological processes and molecular functions overrepresented among the candidate genes. Supervised machine learning algorithms were applied to build classification models using the expression levels of the 20 genes as features. Nested cross-validation was employed to assess model performance. The RF model achieved the highest area under the receiver operating characteristic curve of 0.89, indicating excellent discrimination between PE patients and controls based on the gene expression signature. Validation in larger cohorts is warranted to clinically translate these findings into a non-invasive diagnostic test for PE.

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Assessment of heat shock proteins and endothelial dysfunction in acute pulmonary embolism

Cited by 6 publications

References 33 publications

Cardiac remodelling in a swine model of chronic thromboembolic pulmonary hypertension: comparison of right vs. left ventricle

Cardiac remodelling in a swine model of chronic thromboembolic pulmonary hypertension: comparison of right vs. left ventricle

Endocan as a marker of disease severity in pulmonary thromboembolism

Predicting biomarker for the acute pulmonary embolism by using gene ontology and machine learning

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