Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1301259 | ENA |
REPOSITORIES: ENA
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Project description:In dogs with degenerative mitral valve disease (DMVD), pulmonary hypertension (PH) is a common complication characterized by abnormally elevated pulmonary arterial pressure (PAP). Pulmonary arterial remodeling is the histopathological changes of pulmonary artery that has been recognized in PH. The underlying mechanisms that cause this arterial remodeling are poorly understood. This study aimed to perform shotgun proteomics to investigate changes in protein expression in pulmonary arteries and lung tissues of DMVD dogs with PH compared to normal control dogs and DMVD dogs without PH.
2024-09-09 | PXD045240 | JPOST Repository
Project description:Rationale: Recent studies suggest a potential link between gut bacterial microbiota dysbiosis and PAH, but the exact role of gut microbial communities, including bacteria, archaea, and fungi, in PAH remains unclear. Objectives: To investigate the role of gut microbiota dysbiosis in idiopathic pulmonary arterial hypertension (IPAH) and to assess the therapeutic potential of fecal microbiota transplantation (FMT) in modulating PAH progression. Methods: Using shotgun metagenomics, we analyzed gut microbial communities in IPAH patients and healthy controls. FMT was performed to transfer gut microbiota from IPAH patients or MCT-PAH rats to normal rats and from healthy rats to MCT-PAH rats. Hemodynamic measurements, echocardiography, histological examination, metabolomic and RNA-seq analysis were conducted to evaluate the effects of FMT on PAH phenotypes. Measurements and Main Results: Gut microbiota analysis revealed significant alterations in the bacterial, archaeal, and fungal communities in IPAH patients compared to healthy controls. FMT from IPAH patients induced PAH phenotypes in recipient rats. Conversely, FMT from healthy rats to IPAH rats significantly ameliorated PAH symptoms, restored gut microbiota composition, and normalized serum metabolite profiles. Specific microbial species were identified with high diagnostic potential for IPAH, improving predictive performance beyond individual or combined microbial communities. Conclusions: This study establishes a causal link between gut microbiota dysbiosis and IPAH and demonstrates the therapeutic potential of FMT in reversing PAH phenotypes. The findings highlight the critical role of bacterial, archaeal, and fungal communities in PAH pathogenesis and suggest that modulation of the gut microbiome could be a promising treatment strategy for PAH.
2025-04-30 | GSE271297 | GEO
Project description:<p>Gut microbiota dysbiosis has been implicated in pulmonary arterial hypertension (PAH). However, most studies have focused on the bacterial community and the exact role and mechanisms of multi-kingdom gut microbiota, including bacteria, archaea and fungi in PAH remains largely unclear. Idiopathic PAH (IPAH) patients exhibited distinct gut microbiota profiles with altered bacterial, archaeal and fungal compositions compared to healthy controls. Fecal microbiota transplantation (FMT) from IPAH patients or monocrotaline (MCT)-induced PAH rats to antibiotic treated rats induced PAH phenotypes, including increased right ventricular systolic pressure (RVSP) and pulmonary vascular remodeling. Conversely, FMT from normal rats to MCT-PAH rats ameliorated PAH symptoms and reversed multi-kingdom gut microbiota dysbiosis. Metabolomics revealed significant alterations in plasma metabolites. Our findings established a causal link between multi-kingdom gut microbiota dysbiosis and PAH, demonstrating the therapeutic potential of FMT in reversing PAH phenotypes. More importantly, in addition to gut bacteria, gut archaeal and fungal communities also significantly correlate with PAH pathogenesis, highlighting their indispensable role in the gut.</p>
2025-05-12 | MTBLS10563 | MetaboLights
Project description:Pulmonary hypertension (PH) is a life-threatening disease, characterized by excessive pulmonary vascular remodeling, leading to elevated pulmonary arterial pressure and right heart hypertrophy. PH is caused, among other factors, by chronic hypoxia, leading to hyper-proliferation of pulmonary arterial smooth muscle cells (PASMC) and apoptosis-resistant pulmonary microvascular endothelial cells (PMVEC). Upon re-exposure to normoxia, chronic hypoxia-induced PH in mice is reversible. In this study, we aim to identify novel candidate genes involved in pulmonary vascular remodeling specifically in the pulmonary vasculature.
2022-09-01 | GSE183908 | GEO
Project description:Pulmonary Arterial Hypertension (PAH) is a cardiovascular disease characterized by progressively increasing blood pressure as a result of obliteration and loss of pulmonary arteries. We have extracted pulmonary arterial endothelial cells from lungs of a cohort of PAH patients (n=10) and controls (n=9), cultured the cells for 3-5 passages, and performed chromatin (H3K27ac, H3K4me1, and H3K4me3 ChIP-Seq), expression (RNA-Seq) and chromatin interaction profiling (ChIA-PET). We observed a large-scale remodelling of the active chromatin landscape at enhancers while promoters and gene expression remained unchanged.
2020-03-12 | GSE126322 | GEO
Project description:Pulmonary Arterial Hypertension (PAH) is a cardiovascular disease characterized by progressively increasing blood pressure as a result of obliteration and loss of pulmonary arteries. We have extracted pulmonary arterial endothelial cells from lungs of a cohort of PAH patients (n=10) and controls (n=9), cultured the cells for 3-5 passages, and performed chromatin (H3K27ac, H3K4me1, and H3K4me3 ChIP-Seq), expression (RNA-Seq) and chromatin interaction profiling (ChIA-PET). We observed a large-scale remodelling of the active chromatin landscape at enhancers while promoters and gene expression remained unchanged.
2020-03-12 | GSE139234 | GEO
Project description:Pulmonary hypertension (PH) encompasses a diverse spectrum of disorders characterized by elevated pulmonary arterial pressure presenting substantial morbidity and mortality challenges. Despite significant advancements in understanding its underlying pathophysiology therapeutic options remain limited particularly in cases where patients exhibit elevated pulmonary pressures despite maintaining a preserved left ventricular ejection fraction. The traditional focus on right ventricular (RV) function in PH has led to the underestimation of the impact on the left ventricle (LV) due to the absence of high-resolution modalities capable of monitoring the electromechanical coupling in both ventricles. We present here the results of an integrated histology and transcriptome analysis used to improve our understanding of the pathophysiology of pulmonary hypertension and identify the different molecular responses due to MCT-induced PH.
2025-07-16 | GSE266139 | GEO
Project description:Pulmonary arterial hypertension (PAH) is a progressive disease marked by pulmonary vascular remodeling, elevated pulmonary pressures, and right ventricular (RV) failure. In this study, a sugen-hypoxia rat model of PAH was used to evaluate a novel, degradation-resistant apelin analog targeting the apelinergic pathway, which is implicated in pulmonary vascular remodeling. Treatment with the apelin analog reversed key pathological features of PAH, including pulmonary vascular lesions, elevated pulmonary arterial pressures, RV dilation and dysfunction, and early cardiorenal syndrome. The therapy also reduced RV cardiomyocyte and fibroblast activation caused by pressure overload. Single-nucleus RNA sequencing of the lungs and RV demonstrated that apelin analog treatment activated protective molecular programs, notably restoring balance between protective BMPR2 signaling and pathogenic TGFBR2 signaling. Overall, these findings suggest that exogenous apelin therapy may represent a promising strategy to reverse pulmonary vascular and cardiac remodeling in PAH and warrants further clinical investigation.
2026-05-22 | GSE330160 | GEO
Project description:Pulmonary arterial hypertension (PAH) is characterized by severe obstruction of small pulmonary arteries and concomitant high pulmonary arterial pressure, resulting in progressive right ventricular failure. Previously, we demonstrated that long-term interleukin (IL)-33 administration in mice induced severe occlusive arterial hypertrophy in the lung, which was mediated by group 2 innate lymphoid cells (ILC2s). In response to IL-33, ILC2s accumulated around blood vessels and produced IL-5, leading to perivascular eosinophil recruitment. In this study, we further characterized IL-33-induced pulmonary arterial hypertrophy. We first demonstrated that long-term IL-33 administration caused an increase in the right ventricular pressure. In IL-33 deficient mice, pulmonary arterial hypertrophy mediated by eggs of Schistosoma mansoni (S. mansoni) was attenuated, accompanied with partial reduction in ILC2s, eosinophils and CD4+ T cells. In addition, proteomic analysis revealed dramatic changes in urine samples from mice treated with IL-33 or S. mansoni eggs. Resistin like alpha (RELM), a pulmonary hypertension-related molecule, in the urine was commonly detected in both treatments. Large amounts of RELM were observed in the lung from IL-33-treated mice. These observations support that IL-33-induced pulmonary arterial hypertrophy is a useful model to study the mechanism underlying development of PAH and expolar biomarkers to indicate the onset of PAH.
2024-09-27 | PXD055773 | JPOST Repository
Project description:Pulmonary Arterial Hypertension (PAH) is a cardiovascular disease characterized by progressively increasing blood pressure as a result of obliteration and loss of pulmonary arteries. We have extracted pulmonary arterial endothelial cells from lungs of a cohort of PAH patients (n=10) and controls (n=9), cultured the cells for 3-5 passages, and performed chromatin (H3K27ac, H3K4me1, and H3K4me3 ChIP-Seq), expression (RNA-Seq) and chromatin interaction profiling (ChIA-PET). We observed a large-scale remodelling of the active chromatin landscape at enhancers while promoters and gene expression remained unchanged.
2020-03-12 | GSE126262 | GEO