Clinica chimica acta; international journal of clinical chemistry · 2026
Plasma non-targeted metabolomics unveils the metabolic signatures of trans-right ventricle in pulmonary arterial hypertension associated with atrial septal defect.
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Qian Xifeng, Deng Yuanrui, Guo Tingting, Huang Xin, Yan Chaowu, Gao Xin, Wu Yan, Hu Song, Tan Jiangshan, Chong Lingtao, Zhu Shengsong, Ma Mingjie, Ye Mengting, Wang Xiaojian, Cao Jian, Hua Lu
Аннотация
BACKGROUND: Understanding metabolic evolution of right ventricle (RV) of pulmonary arterial hypertension associated with atrial septal defect (PAH-ASD) helps elucidate the underlying pathobiology and reveal disease-specific biomarkers. However, the exact metabolic profile of RV of PAH-ASD is scarce.
OBJECTIVES: This study aimed to unveil precisely the metabolic signatures of trans-RV of PAH-ASD through non-targeted metabolomics.
METHODS: Participants with PAH-ASD were recruited and their blood samples were obtained from superior vena cava (SVC) and pulmonary artery (PA) through right cardiac catheterization. Non-targeted metabolomics analysis on the basis of UHPLC-MS/MS was utilized to generate the metabolomic signature of trans-RV by comparing the metabolites change from SVC to PA.
RESULTS: 1060 metabolites were detected from blood samples from 40 PAH-ASD participants. A total of 44 differential metabolites were identified based on screening criteria after flowing through the RH, including 10 metabolites with decreased levels and 34 metabolites with increased levels. Among them, phosphatidylcholines, sphingomyelins, AICARP, XMP, inosine 5'-Monophosphate, prostaglandin A1, oleoyl ethanolamide, tyramine, 2-phenylethylamine, 23-nordeoxycholic acid, LPI 20:4, and LPE 22:6 were discovered. Moreover, distinct metabolic perturbations, such as the change of sphingomyelins, inosine 5'-Monophosphate and LPE 22:6, was correlated with the significant clinical variables indicating RV dysfunction in clinical association analysis.
CONCLUSION: Our study correctly defined metabolic signatures indicating towards a metabolic pathogenesis of trans-RV of PAH-ASD, emphasizing the importance of these metabolites in promoting of RV dysfunction and devising therapeutic strategies.
OBJECTIVES: This study aimed to unveil precisely the metabolic signatures of trans-RV of PAH-ASD through non-targeted metabolomics.
METHODS: Participants with PAH-ASD were recruited and their blood samples were obtained from superior vena cava (SVC) and pulmonary artery (PA) through right cardiac catheterization. Non-targeted metabolomics analysis on the basis of UHPLC-MS/MS was utilized to generate the metabolomic signature of trans-RV by comparing the metabolites change from SVC to PA.
RESULTS: 1060 metabolites were detected from blood samples from 40 PAH-ASD participants. A total of 44 differential metabolites were identified based on screening criteria after flowing through the RH, including 10 metabolites with decreased levels and 34 metabolites with increased levels. Among them, phosphatidylcholines, sphingomyelins, AICARP, XMP, inosine 5'-Monophosphate, prostaglandin A1, oleoyl ethanolamide, tyramine, 2-phenylethylamine, 23-nordeoxycholic acid, LPI 20:4, and LPE 22:6 were discovered. Moreover, distinct metabolic perturbations, such as the change of sphingomyelins, inosine 5'-Monophosphate and LPE 22:6, was correlated with the significant clinical variables indicating RV dysfunction in clinical association analysis.
CONCLUSION: Our study correctly defined metabolic signatures indicating towards a metabolic pathogenesis of trans-RV of PAH-ASD, emphasizing the importance of these metabolites in promoting of RV dysfunction and devising therapeutic strategies.