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Gene expression in patients with pulmonary hypertension due to valve heart disease

ABSTRACT: To delve deeper into the molecular mechanisms underlying pulmonary hypertension secondary to left heart disease (PH-LHD), an essential step toward developing a comprehensive classification, reliable biomarkers and targeted therapies. In this study, we analyzed the whole transcriptome (mRNA) of a unique cohort of patients with persistent PH due to valvular heart disease (PH-VHD) to identify biological pathways associated with disease prognosis. The analysis was performed using the well-characterized SIOVAC (Sildenafil for Improving Outcomes after Valvular Correction) clinical trial cohort. We included 116 patients with demonstrated PH-LHD after valvular correction, and 30 VHD patients with no or mild PH (Control).

ORGANISM(S): Homo sapiens

PROVIDER: GSE325715 | GEO | 2026/03/26

REPOSITORIES: GEO

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microRNA expression in patients with pulmonary hypertension due to valve heart disease

Project description:To delve deeper into the molecular mechanisms underlying pulmonary hypertension secondary to left heart disease (PH-LHD). In this study, we analyzed microRNA of a unique cohort of patients with persistent PH due to valvular heart disease (PH-VHD) to identify biological pathways associated with disease prognosis. The analysis was performed using the well-characterized SIOVAC (Sildenafil for Improving Outcomes after Valvular Correction) clinical trial cohort. We included 113 patients with demonstrated PH-LHD after valvular correction, and 30 VHD patients with no or mild PH (Control).

2026-03-24 | GSE325416 | GEO

Comparison of atrial appendage tissues of patients with Valvular Heart Disease and patients with Valvular Heart Disease-Atrial Fibrillation

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2018-04-12 | GSE113013 | GEO

Valvular heart disease and atrial fibrillation regulate microRNA expression profiles in left and right atria differently

Project description:Background: Chronic atrial fibrillation (AF) is a complication associated with the dilated atria of patients with valvular heart disease and contributes to worsened pathology. Methods and Results: Using microarray technology, we examined microRNA (miR) expression profiles in right and left atrial appendage tissue from valvular heart disease (VHD) patients. Right atrial appendage from patients undergoing coronary artery bypass grafting (CABG) and left atrial (LA) appendage from healthy hearts not used for transplant were used as controls. VHD induced different changes in miR expression in LA compared with right atria (RA). Fifty-two (52) miRs were altered by VHD in LA, compared with 5 in RA tissue. There was no detectable effect of chronic AF on miR expression in LA tissue, but miR expression in RA was strongly influenced by AF, with 47 miRs showing differential expression. LA volume correlated with miR expression changes in both LA and RA, but the affected miRs were different for the two atrial groups. Conclusions: VHD and AF influence miR expression patterns in LA and RA, but these are affected differently by disease progression and by the development of AF. These findings provide new insights into the progression of VHD. RA tissue is not a useful surrogate for LA in studies of mitral valve disease. 34 arrays from either the left or right atrium from patients with Valvular Heart Disease (VHD), patients undergoing coronary artery bypass grafting (CABG), or healthy controls. Arrays in this series were generated on V2 and V3 Agilent microRNA arrays and analysed in combination.

2011-12-21 | E-GEOD-28954 | biostudies-arrayexpress

Valvular heart disease and atrial fibrillation regulate microRNA expression profiles in left and right atria differently

2011-12-21 | GSE28954 | GEO

Cellular landscapes of non-diseased human cardiac valves from end-stage heart failure-explanted heart

Project description:Exploring the mechanisms of valvular heart disease (VHD) at the cellular level may be useful to identify new therapeutic targets; however, the comprehensive cellular landscape of non-diseased human cardiac valve leaflets remains unclear. The cellular landscapes of non-diseased human cardiac valve leaflets (five aortic valves, five pulmonary valves, five tricuspid valves, and three mitral valves) from end-stage heart failure patients undergoing heart transplantation were explored using single-cell RNA sequencing (scRNA-seq)

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Comparison of atrial appendage tissues of patients with Valvular Heart Disease and patients with Valvular Heart Disease-Atrial Fibrillation

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MADSCAN evaluation using heart disease patients

Project description:Data set for microarray data processing tool evaluation. Patients affected by valvular heart disease and coronary artery disease, or idiopathic dilated cardiomyopathy. Keywords = Myochip Keywords = MADSCAN Keywords: other

2004-07-02 | GSE1502 | GEO

Metabolomics Characterization of Human Calcific Aortic Valve Stenosis

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2020-02-03 | MTBLS1267 | MetaboLights

Pluripotent stem cell-based screening uncovers sildenafil as a mitochondrial disease therapy

Project description:Mitochondrial disease encompasses inherited disorders affecting mitochondrial function. A severe and untreatable form of mitochondrial disease is Leigh syndrome (LS) causing psychomotor regression and metabolic crises. To accelerate drug discovery for LS, we screen a library of 5,632 repurposable compounds in neural cells from LS patient-derived induced pluripotent stem cells (iPSCs). We identify phosphodiesterase 5 (PDE5) inhibitors as leads and prioritize sildenafil for its clinical safety. Sildenafil corrects mitochondrial membrane potential defects, restores neurodevelopmental pathways, and normalizes calcium responses in LS brain organoids. In small and large mammalian models of LS, sildenafil extends the lifespan and ameliorates disease phenotypes. Off-label individual basis treatment with sildenafil in six LS patients improves their motor function and resistance to metabolic crises. Collectively, the findings highlight the potential of iPSC-driven drug discovery and position sildenafil as a promising drug candidate for mitochondrial disease.

2026-02-09 | PXD059519 | Pride

Reprogramming-driven drug discovery uncovers sildenafil as a candidate drug for mitochondrial disease

Project description:Mitochondrial disease is a group of rare inherited conditions affecting mitochondrial function. A severe untreatable form of mitochondrial disease is Leigh syndrome (LS) characterized by psychomotor regression and acute metabolic crises. To accelerate drug discovery for mitochondrial disease, we focused on drug repurposing and made use of induced pluripotent stem cell (iPSC)-derived neuronal precursor cells (NPCs) from LS patients to screen a library of 5,632 repurposable compounds. We identified phosphodiesterase 5 inhibitors (PDE5i) as leads capable of normalizing mitochondrial polarization in LS NPCs. Among PDE5i, we prioritized Sildenafil due to its established safety profile in children. Sildenafil restored key pathways regulating nervous system development, enhanced neurite outgrowth in LS neurons, and mitigated abnormal calcium responses in LS brain organoids under metabolic stress. In a mouse model of LS, Sildenafil led to lifespan extension and amelioration of metabolic and encephalopathy phenotypes. Lastly, chronic off-label treatment with Sildenafil in six LS patients demonstrated good tolerability and clinical improvements. Our findings highlight the potential of iPSC-driven drug discovery for rare diseases and position Sildenafil as a promising candidate drug for patients with mitochondrial disease.

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