Alterations in gut microbiota and plasma metabolites in pulmonary arterial hypertension secondary to congenital left-to-right shunt heart disease: potential mechanisms and biomarkers

先天性左向右分流性心脏病继发肺动脉高压患者肠道菌群和血浆代谢物的变化:潜在机制和生物标志物

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Abstract

INTRODUCTION: Pulmonary arterial hypertension (PAH) secondary to congenital left-to-right shunt heart disease (CL-RSHD) is a life-threatening complication with unclear microbial and metabolic mechanisms. This study investigated gut microbiota and plasma metabolic alterations in CL-RSHD-associated PAH to identify biomarkers and mechanistic pathways. METHODS: This cross-sectional study included 86 participants: healthy controls (HC, n = 13), CL-RSHD (n = 46), and CL-RSHD + PAH (n = 27). Gut microbiota was analyzed using 16S rRNA gene sequencing of the V3-V4 region on 41 fecal samples (HC, n = 9; CL-RSHD, n = 15; and CL-RSHD + PAH, n = 17). Untargeted plasma metabolomics was analyzed on all 86 plasma samples. Microbial diversity, differential taxa (DESeq2), metabolic pathways (OPLS-DA, KEGG), and biomarker potential (ROC curves) were assessed. Dynamic correlations linked microbiota-metabolite interactions. RESULTS: CL-RSHD + PAH patients showed preserved α/β-diversity but distinct taxonomic shifts: enriched Lachnoclostridium phocaeense (Firmicutes) and reduced SCFA-producing Anaerostipes. Metabolomics revealed dysregulated steroid biosynthesis, cortisol metabolism, and oxidative stress pathways. Key metabolites, including elevated 5-hydroxymethylcytidine (5-hmC) and γ-L-glutamyl-L-cysteine, and reduced histidine intermediate D-E1IG3P, correlated with PAH severity. Strong microbiota-metabolite interactions (e.g., Lactonifactor-D-E1IG3P, r = 0.82, P < 0.01) suggested a disrupted vascular remodeling axis. Metabolites like ADP-glucose (AUC = 0.94) and 3-phenylpropyl glucosinolate (AUC = 0.92) showed high diagnostic accuracy. CONCLUSION: CL-RSHD-associated PAH involves gut microbial restructuring and metabolic reprogramming linked to immune-inflammatory activation and oxidative stress. The Firmicutes-histidine metabolism axis emerges as a therapeutic target. Despite limitations, this study provides foundational insights into microbial-metabolic drivers of PAH, highlighting novel biomarkers for early diagnosis and intervention.

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