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pmid:40677372

Bioinformatics Analysis Identifies a Potential Key Gene in the Pathogenesis of Pulmonary Hypertension-HSPH1.

Yuelong Ji · Xia Li · Rui Wang · Zhongsu Wang · Guangdong Yu · Conghu Yuan · Xiangnan Li

Pulmonary circulation · 2025 doi:10.1002/pul2.70127

Paper

complete

Experiment

complete

Data

partial

Analysis

partial

Execution

absent

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title
Bioinformatics Analysis Identifies a Potential Key Gene in the Pathogenesis of Pulmonary Hypertension-HSPH1.
doi
10.1002/pul2.70127
pmid
40677372
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Yuelong Ji
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Xia Li
[2]
Rui Wang
[3]
Zhongsu Wang
[4]
Guangdong Yu
[5]
Conghu Yuan
[6]
Xiangnan Li
journal
Pulmonary circulation
year
2025
abstract
Pulmonary arterial hypertension (PAH) is a progressive vascular disease characterized by small artery occlusion, increased pulmonary vascular resistance, and right heart failure. HSPH1, a member of the heat shock protein family, has been shown to inhibit protein aggregation but its role in PAH remains unclear. The purpose of this study was to explore the expression pattern and potential mechanism of HSPH1 in PAH, and to provide new diagnostic markers for PAH. In the study differentially expressed genes from two GEO microarray datasets (GSE53408, GSE113439) were analyzed to identify potential biomarkers for PAH. The expression of HSPH1 in normal lung tissue and pulmonary hypertension tissue was verified by bioinformatics and various experiments. This study also validated the potential mechanism of action of HSPH1 in PAH through transfection techniques. In addition, clinical correlation analysis was used to verify whether HSPH1 was correlated with clinical indicators (age, smoking history, hypertension, SII, NLR, PLR). The results showed that the protein level of HSPH1 was significantly increased in the pulmonary artery tissue of rats with pulmonary hypertension. In the plasma of patients with clinical PAH, the expression of HSPH1 mRNA was also observed to be significantly increased, and its expression was also associated with inflammatory markers such as NLR, PLR and SII. In addition, wet experiments found that HSPH1 could promote the proliferation of pulmonary artery smooth muscle cells, promote epithelial-mesenchymal transformation and inhibit apoptosis. These findings suggest that HSPH1 plays a crucial role in PAH progression and may serve as a potential diagnostic biomarker for the disease.
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The data set was independently analyzed, and background correction, percentiles normalization, and log2 transformation were performed using the GEO2R default process (based on the limma package). Because the data set sources were independent and the platform was the same, the ComBat algorithm (R package sva) was used to correct the batch effect.
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These findings suggest that HSPH1 plays a crucial role in PAH progression and may serve as a potential diagnostic biomarker for the disease.
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differentially expressed genes from two GEO microarray datasets (GSE53408, GSE113439) were analyzed
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HSPH1, a member of the heat shock protein family, has been shown to inhibit protein aggregation but its role in PAH remains unclear. The purpose of this study was to explore the expression pattern and potential mechanism of HSPH1 in PAH, and to provide new diagnostic markers for PAH. In the study differentially expressed genes from two GEO microarray datasets (GSE53408, GSE113439) were analyzed to identify potential biomarkers for PAH. The expression of HSPH1 in normal lung tissue and pulmonary hypertension tissue was verified by bioinformatics and various experiments. This study also validated the potential mechanism of action of HSPH1 in PAH through transfection techniques. In addition, clinical correlation analysis was used to verify whether HSPH1 was correlated with clinical indicators (age, smoking history, hypertension, SII, NLR, PLR). 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