Exploring the biological basis for the identification of different syndromes in ischemic heart failure based on joint multi-omics analysis
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PROVIDER: PRJNA1294199 | ENA |
REPOSITORIES: ENA
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Project description:IHF is a major chronic disease that seriously threatens human health. Qi deficiency and blood stasis syndrome (QDBS), Yang deficiency with blood stasis syndrome (YDBS) and Yang deficiency and blood stasis with fluid retention syndrome (YDBSFR) are the basic syndromes of IHF in Chinese medicine. This study aims to explore the biological basis of the three IHF syndromes through integrated multi-omics research. We analyzed and integrated transcriptomic, proteomic, and targeted metabolomic data from IHF patients and healthy persons to obtain the key biomarkers and enriched pathways of QDBS, YDBS and YDBSFR(Registration No.: ChiCTR2200058314). These biomarkers were combined with clinical indicators to construct the "Disease-Syndromes-Clinical phenotypes-Biomarkers-Pathways" network, and the obtained differential genes and proteins were externally validated. The potential biomarkers for QDBS included SDHD, IL10, ACTG1, VWF, MDH2, COX5A, Valeric acid, Succinic Acid and L-Histidine, which were predominantly enriched in TCA cycle, oxidative phosphorylation, platelet activation, and neutrophil extracellular trap formation pathways, demonstrating associations with energy metabolism, coagulation system, and immune-inflammatory responses.YDBS potential biomarkers included TSHR, PRKG1, ATP1A2, GNAI2, APOA2, PLTP, 3-Hydroxybutyrate, Hexadecanoic acid and Palmitelaidic acid, and the combined pathways were mainly enriched in thyroid hormone synthesis, regulation of lipolysis in adipocytes, cholesterol metabolism and PPAR signaling pathways, correlating with hormonal regulation and lipid metabolism. The potential biomarkers of YDBSFR were CNGB1, KCNMA1, PIK3R2, HSPA8, C3, FH, Oxamic acid, N-Acetyl-L-alanine, 4-Hydroxyhippuric acid, and the combined pathways were mainly enriched in aldosterone-regulated sodium reabsorption, cGMP-PKG signaling pathway, neutrophil extracellular trap formation and TCA cycle signaling pathways, which are related to hormone regulation, signal transduction, immune-inflammatory response and energy metabolism. Platelet activation was involved in the whole process of IHF. External validation demonstrated the above core targets. This study investigated the biological basis of QDBS, YDBS and YDBSFR in IHF from a modern biomedical perspective, providing references for the objective research of TCM syndrome differentiation.
2025-08-01 | GSE303117 | GEO
Project description:Inherited Bone Marrow Failure Syndromes
| PRJNA417131 | ENA
Project description:Inherited Bone Marrow Failure Syndromes
| PRJNA417130 | ENA
Project description:We characterized the metabolic and cardiac mitochondrial function in a mouse model of non-ischemic HF. Inhibition of nitric oxide synthesis and hypertension, which often present together, are two important risk factors in human non-ischemic HF. Compared with L-NAME L-NG-Nitroarginine methyl ester (L-NAME), an inhibitor of nitric oxide synthesis or Angiotensin II (AngII), a hypertensive agent treatment alone, L-NAME+AngII induced the most severe HF phenotype characterized by edema, hypertrophy, fibrosis, increased blood pressure and reduced ejection fractions. L-NAME+AngII treated mice had robust deterioration of cardiac mitochondrial function we observed. Microarray analyses revealed majority of the gene changes attributed to the combination of L-NAME+AngII. Pathway analyses indicated significant changes in metabolic pathways such as mitochondrial oxidative phosphorylation, fatty acid metabolism and tricarboxylic acid pathways etc.in L-NAME+AngII hearts. We conclude that combination of L-NAME+AngII exacerbates cardiac contractile and mitochondrial functional de-regulation compared with L-NAME and AngII alone, resulting in non-ischemic HF. This model of heart failure may be highly valuable in studying mechanisms and treatments for non-ischemic heart failure. Twelve week-old C57BL6 male mice were randomly assigned to 4 groups: 1. Control, 2. L-NAME treatment, 3. AngII treatment, 4. L-NAME+AngII treatment.L-NAME (0.3 mg/ml with 1% NaCl) was administered in drinking water. AngII (0.7 mg/kg/day) was administered via subcutaneous micro-osmotic pumps. L-NAME and AngII were administered to mice for 5 weeks and 4 weeks in combination to induce HF or alone to study the effects of the individual agents.
2016-01-19 | E-GEOD-72132 | biostudies-arrayexpress
Project description:Heart failure is a leading cause of cardiovascular mortality with limited options for treatment. We analyzed whether the anti-ischemic drug ranolazine could retard the progression of heart failure in an experimental model of heart failure induced by 6 months of chronic pressure overload. The study showed that 2 months of ranolazine treatment improved cardiac function of aortic constricted C57BL/6J (B6) mice with symptoms of heart failure as assessed by echocardiography. The microarray gene expression study of heart tissue from failing hearts relative to ranolazine-treated and healthy control hearts identified heart failure-specific genes that were normalized during treatment with the anti-ischemic drug ranolazine. Microarray gene expression profiling was performed with heart tissue isolated from three study groups: (i) untreated 10 month-old C57BL/6J (B6) mice with heart failure induced by 6 months of abdominal aortic constriction (AAC), (ii) 10 month-old B6 mice with 6 months of AAC and two months of treatment with the anti-ischemic drug ranolazine (200 mg/kg), and (iii) age-matched, untreated, sham-operated B6 control mice.
2010-12-03 | E-GEOD-25766 | biostudies-arrayexpress
Project description:We characterized the metabolic and cardiac mitochondrial function in a mouse model of non-ischemic HF. Inhibition of nitric oxide synthesis and hypertension, which often present together, are two important risk factors in human non-ischemic HF. Compared with L-NAME L-NG-Nitroarginine methyl ester (L-NAME), an inhibitor of nitric oxide synthesis or Angiotensin II (AngII), a hypertensive agent treatment alone, L-NAME+AngII induced the most severe HF phenotype characterized by edema, hypertrophy, fibrosis, increased blood pressure and reduced ejection fractions. L-NAME+AngII treated mice had robust deterioration of cardiac mitochondrial function we observed. Microarray analyses revealed majority of the gene changes attributed to the combination of L-NAME+AngII. Pathway analyses indicated significant changes in metabolic pathways such as mitochondrial oxidative phosphorylation, fatty acid metabolism and tricarboxylic acid pathways etc.in L-NAME+AngII hearts. We conclude that combination of L-NAME+AngII exacerbates cardiac contractile and mitochondrial functional de-regulation compared with L-NAME and AngII alone, resulting in non-ischemic HF. This model of heart failure may be highly valuable in studying mechanisms and treatments for non-ischemic heart failure.
2016-01-19 | GSE72132 | GEO
Project description:LCMS files from tryptic digests of ~1-4 mg piece of heart ventricular tissue from human with ischemic heart failure and non-failing controls.
Specimen number correspond to .raw files as follows:
Ischemic Heart failure -
54687.1; HF_1_phos.raw
53148.1; HF_2_phos.raw
53589.2; HF_3_phos.raw
54146.1; HF_4_phos.raw
52935.1; HF_5_phos.raw
Non-failing -
52941.1; NHF_1_phos.raw
52777.1; NHF_2_phos.raw
53019.2; NHF_3_phos.raw
53058.1; NHF_4_phos.raw
52621.1; NHF_5_phos.raw
2022-12-07 | MSV000090858 | MassIVE
Project description:Acute renal failure (ARF) has high morbidity and mortality. In animal ARF models, effective treatments must be administered before or shortly after the insult, limiting their clinical potential. We used microarrays to identify early biomarkers that distinguish ischemic from nephrotoxic ARF, or that detect both injury types. We compared rat kidney transcriptomes 2 and 8 hours after ischemia/reperfusion and after mercuric chloride. Quality control and statistical analyses were necessary to normalize inter-experimental groups, eliminate outliers, and exclude unaltered genes. Principal component analysis revealed distinct ischemic and nephrotoxic trajectories, and clear array groupings. Therefore, we used supervised analysis, t-tests and fold changes, to compile gene lists for each group, exclusive or non-exclusive, alone or in combination. We used two lots of microarrays (Lot 1, n = 24, Lot 2, n = 12), for a total of 36 microarrays. Five of them were duplicates, where two aliquots of RNA from the same rat were processed independently and hybridized to separate microarrays. Normal rats were used in both lots (n = 3 for each lot) for normalization.
2010-07-01 | E-GEOD-3219 | biostudies-arrayexpress
Project description:Exploring biomarkers based on ischemic stroke proteomics studies
2022-10-27 | PXD036840 |
Project description:ZRSR2 mutant myelodysplastic syndromes
| PRJNA671387 | ENA