Circulating immune cell signature analysis in HFpEF across species [RNA-Seq - mouse]
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ABSTRACT:
PROVIDER: PRJNA1268464 | ENA |
REPOSITORIES: ENA
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Project description:Circulating immune cell signature analysis in HFpEF across species
| PRJNA1268490 | ENA
Project description:Circulating immune cell signature analysis in HFpEF across species [RNA-Seq - human]
| PRJNA1268463 | ENA
Project description:Circulating immune cell signature analysis in HFpEF across species [scRNA-Seq - mouse]
| PRJNA1268466 | ENA
Project description:Background: HFpEF is a heterogeneous clinical picture that is closely related to extracardiac comorbidities such as obesity, hypertension and diabetes and is associated with chronic, low-grade systemic inflammation. Previous studies on myocardial biopsies of HFpEF patients showed intramyocardial inflammatory activity, suggesting that the inflammatory processes in HFpEF are predominantly systemic and exhibit compartment specific-patterns. Methods: We performed single cell RNA sequencing (scRNA-seq) of peripheral blood mononuclear cells (PBMCs) of HFpEF patients (n=6), HFrEF patients (n=8) and healthy controls (n=7) taking obesity status into account. For validation, bulk RNA sequencing was performed on whole blood samples. In parallel, the systemic immune cell response was investigated in a HFpEF mouse model (induced by a high-fat diet plus L-NAME), with one group additionally administered the anti-inflammatory agent nitro-oleic acid (NO₂-OA). Results: Analysis of human PBMCs revealed a HFpEF-specific inflammatory fingerprint, which manifested in obesity-related increased expression of cytokine signaling genes (e.g. CCL2, TNF) and obesity-independent increases in mitochondrial-associated activity. In the mouse model, HFpEF animals showed a comparable increase in inflammatory markers, with treatment with NO₂-OA leading to a partial normalization of immunological signatures and a significant improvement in diastolic function. Conclusion: Our results demonstrate that the immune cells of patients with HFpEF are characterized by a distinct transcriptional immune signature that differs from that of patients with HFrEF. The conserved immunological signatures between humans and mice, and the beneficial effect of NO₂-OA in a preclinical model, provide important translational insights and generate hypotheses for personalized interventions in HFpEF.
2025-07-28 | GSE298173 | GEO
Project description:Background: HFpEF is a heterogeneous clinical picture that is closely related to extracardiac comorbidities such as obesity, hypertension and diabetes and is associated with chronic, low-grade systemic inflammation. Previous studies on myocardial biopsies of HFpEF patients showed intramyocardial inflammatory activity, suggesting that the inflammatory processes in HFpEF are predominantly systemic and exhibit compartment specific-patterns. Methods: We performed single cell RNA sequencing (scRNA-seq) of peripheral blood mononuclear cells (PBMCs) of HFpEF patients (n=6), HFrEF patients (n=8) and healthy controls (n=7) taking obesity status into account. For validation, bulk RNA sequencing was performed on whole blood samples. In parallel, the systemic immune cell response was investigated in a HFpEF mouse model (induced by a high-fat diet plus L-NAME), with one group additionally administered the anti-inflammatory agent nitro-oleic acid (NO₂-OA). Results: Analysis of human PBMCs revealed a HFpEF-specific inflammatory fingerprint, which manifested in obesity-related increased expression of cytokine signaling genes (e.g. CCL2, TNF) and obesity-independent increases in mitochondrial-associated activity. In the mouse model, HFpEF animals showed a comparable increase in inflammatory markers, with treatment with NO₂-OA leading to a partial normalization of immunological signatures and a significant improvement in diastolic function. Conclusion: Our results demonstrate that the immune cells of patients with HFpEF are characterized by a distinct transcriptional immune signature that differs from that of patients with HFrEF. The conserved immunological signatures between humans and mice, and the beneficial effect of NO₂-OA in a preclinical model, provide important translational insights and generate hypotheses for personalized interventions in HFpEF.
2025-07-28 | GSE298172 | GEO
Project description:Background: HFpEF is a heterogeneous clinical picture that is closely related to extracardiac comorbidities such as obesity, hypertension and diabetes and is associated with chronic, low-grade systemic inflammation. Previous studies on myocardial biopsies of HFpEF patients showed intramyocardial inflammatory activity, suggesting that the inflammatory processes in HFpEF are predominantly systemic and exhibit compartment specific-patterns. Methods: We performed single cell RNA sequencing (scRNA-seq) of peripheral blood mononuclear cells (PBMCs) of HFpEF patients (n=6), HFrEF patients (n=8) and healthy controls (n=7) taking obesity status into account. For validation, bulk RNA sequencing was performed on whole blood samples. In parallel, the systemic immune cell response was investigated in a HFpEF mouse model (induced by a high-fat diet plus L-NAME), with one group additionally administered the anti-inflammatory agent nitro-oleic acid (NO₂-OA). Results: Analysis of human PBMCs revealed a HFpEF-specific inflammatory fingerprint, which manifested in obesity-related increased expression of cytokine signaling genes (e.g. CCL2, TNF) and obesity-independent increases in mitochondrial-associated activity. In the mouse model, HFpEF animals showed a comparable increase in inflammatory markers, with treatment with NO₂-OA leading to a partial normalization of immunological signatures and a significant improvement in diastolic function. Conclusion: Our results demonstrate that the immune cells of patients with HFpEF are characterized by a distinct transcriptional immune signature that differs from that of patients with HFrEF. The conserved immunological signatures between humans and mice, and the beneficial effect of NO₂-OA in a preclinical model, provide important translational insights and generate hypotheses for personalized interventions in HFpEF.
2025-07-28 | GSE298171 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2025-07-28 | GSE298197 | GEO
Project description:Immune cell activation in heart failure is poorly understood. We profiled circulating leukocytes in humans with heart failure with preserved ejection fraction and non heart failure controls to identify novel changes associated with HFpEF diagnosis
2024-09-01 | GSE223527 | GEO
Project description:Microvascular dysfunction is an important determinant in HFpEF but the role of mural cells herein is still poorly investigated. We aimed to examine the transcriptomic signature of endothelial cells and mural cells of the micro- and macrovascular niche in healthy vs. HFpEF cell RNAsequencing.
2025-02-10 | GSE263197 | GEO
Project description:In this study, we compared the expression profiles of circulating miRNAs in blood samples from controls and patients with heart ailment. Subject with no past history of heart failure/disease are considered as controls. The patients were classified according to the percentage of left ventricular ejection fraction. Patients were grouped as heart failure with reduced (hfREF) and preserved (hfPEF) left ventricular ejection fraction. Employing miRNA microarray, we identified 'signature miRNAs' in peripheral blood samples that distinguished Heart failure from the non-heart failure controls, as well as those of hfREF and hfPEF groups.
2015-02-12 | GSE53437 | GEO