Whole blood transcriptomic profiling in men and women with heart failure
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA750774 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Background. Chronic Heart Failure (CHF) is a systemic syndrome with a poor prognosis and a need for novel therapies. We investigated whether whole-blood transcriptomic profiling can provide new mechanistic insights into CHF. Baseline whole-blood transcriptome profiles were generated from 944 CHF patients from the BIOSTAT-CHF Study.
2023-03-01 | GSE181114 | GEO
Project description:RELEVANCE: Identifying early plasma protein biomarkers that predict the development of heart failure (HF) following myocardial infarction (MI) will help to stratify at risk subjects and provide insight into more effective therapeutic strategies. OBJECTIVE/HYPOTHESIS: The goal of this study was to determine markers of HF in African Americans, using plasma samples collected before the development of symptoms. We propose that early plasma glycoprotein changes will link to later development of heart failure. ApolipoproteinF will be the strongest indicator. METHODS: Plasma samples from a subset of Jackson Heart Study participants with a history of MI but without prevalent heart failure (HF) at visit 2 (2005-2008) were analyzed by glycoproteomics. Individuals were grouped into those who experienced subsequent HF hospitalization after visit 2 (n=15; 3 men/ 12 women) and those without HF hospitalization through 2012 (n=45; 24 men/ 21 women). N-linked plasma glycopeptides were quantified by solid-phase extraction coupled to mass spectrometry and identified using RefSeq and SwissProt. Proteins were mapped for biological processes and functional pathways using Ingenuity Pathway Analysis (IPA) and linked to clinical characteristics.
2018-08-30 | PXD009870 | Pride
Project description:Muscle biopsies taken from vastus lateralis muscle of 15 men and 15 women after 3 days of standardized diet and activity to examine effects of sex and age Subjects were either young adults (7 men and 7 women, 20-29 yr old) or older (8 men and 8 women, 65-75 yr old) Affymetrix U133A and U133B arrays were scanned both before (S1) and after (S2) antibody enhancement. This file has U133A S1 data. Effects of age were computed for men and women separately with an alternative method previously and data submitted as GSE362 (men) and GSE674 (women). Keywords: sex differences, age-related differences
2007-11-24 | GSE9676 | GEO
Project description:Profile of small RNA contents of plasma Evs in men and women at rest and after a bout of acute resistance exercise both before and after 12 weeks of chronic resistance exercise training. We profile how acute and chronic weight training imapcts EV small RNA contents and how this differs in men and women.
2023-06-30 | GSE232700 | GEO
Project description:FASILOX analysis of heart and lung tissue form mice with heart failure with preserved ejection fraction and several comorbidities.
2024-10-02 | PXD056447 | JPOST Repository
Project description:Heart failure is a prevalent condition that affects millions of people worldwide with men exhibiting a higher incidence than women. However, the mechanisms underlying this sex difference remain poorly understood. Our previous work has shown that the presence of mosaic loss of Y chromosome (LOY) in leukocytes is causally associated with increased risk for heart failure. In the current study, we show that LOY macrophages from the failing hearts of humans with dilated cardiomyopathy exhibit widespread changes in gene expression that correlate with fibroblast activation in the myocardium, and we identify the ubiquitously transcribed tetratricopeptide Y linked (Uty) gene in leukocytes as a causal locus for accelerated progression of heart failure in male mice with LOY. Using single-cell multiomics analysis, we demonstrate that Uty disruption leads to epigenetic alterations in both monocytes and macrophages, increasing the propensity of differentiation into pro-fibrotic macrophages that can contribute to cardiac fibrosis and dysfunction. These findings shed light on the mechanisms that contribute to the higher incidence of heart failure in males and suggest potential targets for treatment of heart failure patients with LOY in leukocytes.
2024-01-22 | GSE241486 | GEO
Project description:Hematopoietic mosaic loss of Y chromosome (mLOY) is associated with increased risk of mortality and a variety of age-related diseases in men, but causal and mechanistic relationships have yet to be established. Here it is shown that mice reconstituted with bone marrow cells lacking the Y chromosome display increased mortality and age-related profibrotic pathologies including a progressive decline in cardiac function. Accelerated cardiac dysfunction and fibrosis were also observed in younger mice subjected to a pressure-overload model of heart failure. Bone marrow-derived, cardiac macrophages lacking the Y chromosome exhibited polarization toward a more fibrotic and less inflammatory phenotype. Treatment with a TGFb1 neutralizing antibody led to greater amelioration of heart failure in mice reconstituted with mLOY compared to wild-type bone marrow. Consistent with these data, a prospective study in men revealed that mLOY in blood is associated with an increased risk for cardiovascular disease and heart failure-associated mortality. Together, these results indicate that hematopoietic mLOY contributes to heart failure in men.
2022-08-01 | GSE204732 | GEO
Project description:Hematopoietic mosaic loss of Y chromosome (mLOY) is associated with increased risk of mortality and a variety of age-related diseases in men, but causal and mechanistic relationships have yet to be established. Here it is shown that mice reconstituted with bone marrow cells lacking the Y chromosome display increased mortality and age-related profibrotic pathologies including a progressive decline in cardiac function. Accelerated cardiac dysfunction and fibrosis were also observed in younger mice subjected to a pressure-overload model of heart failure. Bone marrow-derived, cardiac macrophages lacking the Y chromosome exhibited polarization toward a more fibrotic and less inflammatory phenotype. Treatment with a TGFb1 neutralizing antibody led to greater amelioration of heart failure in mice reconstituted with mLOY compared to wild-type bone marrow. Consistent with these data, a prospective study in men revealed that mLOY in blood is associated with an increased risk for cardiovascular disease and heart failure-associated mortality. Together, these results indicate that hematopoietic mLOY contributes to heart failure in men.
2022-06-02 | GSE205090 | GEO
Project description:Hematopoietic mosaic loss of Y chromosome (mLOY) is associated with increased risk of mortality and a variety of age-related diseases in men, but causal and mechanistic relationships have yet to be established. Here it is shown that mice reconstituted with bone marrow cells lacking the Y chromosome display increased mortality and age-related profibrotic pathologies including a progressive decline in cardiac function. Accelerated cardiac dysfunction and fibrosis were also observed in younger mice subjected to a pressure-overload model of heart failure. Bone marrow-derived, cardiac macrophages lacking the Y chromosome exhibited polarization toward a more fibrotic and less inflammatory phenotype. Treatment with a TGFb1 neutralizing antibody led to greater amelioration of heart failure in mice reconstituted with mLOY compared to wild-type bone marrow. Consistent with these data, a prospective study in men revealed that mLOY in blood is associated with an increased risk for cardiovascular disease and heart failure-associated mortality. Together, these results indicate that hematopoietic mLOY contributes to heart failure in men.
2022-06-02 | GSE205089 | GEO