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Dataset results
116 results for “cardiac fibrosis”
Activation of imprinted gene Pw1 promotes cardiac fibrosis after ischemic injury [control_and_Pw1 CKO]
GEO Series GSE232326. Mus musculus. 11 samples. Type: Expression profiling by high throughput sequencing.
Sodium myo-inositol cotransporter-1, SMIT1, promotes cardiac hypertrophy and fibrosis in pressure overloaded mouse hearts
GEO Series GSE245135. Mus musculus. 10 samples. Type: Expression profiling by high throughput sequencing.
Expression profiles and bioinformatic analysis of circRNAs in cardiac fibrosis of db/db mice
GEO Series GSE239970. Mus musculus. 6 samples. Type: Non-coding RNA profiling by array.
Long noncodng RNA lncPostn links TGF-b and p53 signaling pathwas to regulate cardiac fibrosis
GEO Series GSE184342. Mus musculus. 10 samples. Type: Expression profiling by array; Non-coding RNA profiling by array.
FTO suppresses cardiac fibrosis after myocardial infarction via m6A-mediated epigenetic modification [MeRIP-seq]
GEO Series GSE259328. Rattus norvegicus. 4 samples. Type: Methylation profiling by high throughput sequencing.
Single nucleus RNA sequencing and functional in vivo studies reveal TCF21 as a protective regulator in cardiac fibrosis
GEO Series GSE270517. Homo sapiens. 7 samples. Type: Expression profiling by high throughput sequencing.
FTO suppresses cardiac fibrosis after myocardial infarction via m6A-mediated epigenetic modification
GEO Series GSE257546. Rattus norvegicus. 6 samples. Type: Expression profiling by high throughput sequencing.
Macrophage-derived Chemokine (C-C motif) ligand 24 (CCL24) promotes cardiac fibrosis
GEO Series GSE300219. Mus musculus. 14 samples. Type: Expression profiling by high throughput sequencing.
Partial dataset related to the article: "Fibrosis Rescue Improves Cardiac Function in Dystrophin-Deficient Mice and Duchenne Patient-Specific Cardiomyocytes by Immunoproteasome Modulation".
<p>This record contains raw data related to the article: "Fibrosis Rescue Improves Cardiac Function in Dystrophin-Deficient Mice and Duchenne Patient-Specific Cardiomyocytes by Immunoproteasome Modulation".</p> <p>Abstract</p> <p>Patients affected by Duchenne muscular dystrophy (DMD) develop a progressive dilated cardiomyopathy<br> characterized by inflammatory cell infiltration, necrosis, and cardiac fibrosis. Standard<br> treatments consider the use of b-blockers and angiotensin-converting enzyme inhibitors that are<br> symptomatic and unspecific toward DMD disease. Medications that target DMD cardiac fibrosis are<br> in the early stages of development. We found immunoproteasome dysregulation in affected hearts<br> of mdx mice (murine animal model of DMD) and cardiomyocytes derived from induced pluripotent<br> stem cells of patients with DMD. Interestingly, immunoproteasome inhibition ameliorated cardiomyopathy<br> in mdx mice and reduced the development of cardiac fibrosis. Establishing the<br> immunoproteasome inhibitionedependent cardioprotective role suggests the possibility of modulating<br> the immunoproteasome as new and clinically relevant treatment to rescue dilated cardiomyopathy<br> in patients with DMD.</p>
Soluble Receptor for Advanced Glycation End-products regulates age-associated Cardiac Fibrosis
<p>This record contains raw data related to the article "Soluble Receptor for Advanced Glycation End-products regulates age-associated Cardiac Fibrosis"</p> <p>Myocardial aging increases the cardiovascular risk in the elderly. The Receptor for Advanced Glycation End-products (RAGE) is involved in age-related disorders. The soluble isoform (sRAGE) acts as a scavenger blocking the membrane-bound receptor activation. This study aims at investigating RAGE contribution to age-related cardiac remodeling. We analyzed the cardiac function of three different age groups of female <em>Rage-/-</em> and C57BL/6N (WT) mice: 2.5- (Young), 12- (Middle-age, MA) and 21-months (Old) old. While aging, <em>Rage-/-</em> mice displayed an increase in left ventricle (LV) dimensions compared to age-matched WT animals, with the main differences observed in the MA groups. <em>Rage-/-</em> mice showed higher fibrosis and a larger number of α-Smooth Muscle Actin (SMA)+ cells with age, along with increased expression of pro-fibrotic Transforming Growth Factor (TGF)-β1 pathway components. RAGE isoforms were undetectable in LV of WT mice, nevertheless, circulating sRAGE declined with aging and inversely associated with LV diastolic dimensions. Human cardiac fibroblasts stimulated with sRAGE exhibited a reduction in proliferation, pro-fibrotic proteins and TGF-beta Receptor 1 (TGFbR1) expression and Smad2-3 activation. Finally, sRAGE administration to MA WT animals reduced cardiac fibrosis. Hence, our work shows that RAGE associates with age-dependent myocardial changes and indicates sRAGE as an inhibitor of cardiac fibroblasts differentiation and age-dependent cardiac fibrosis.</p>
Dataset related to the article "Reduction of Cardiac Fibrosis by Interference With YAP-Dependent Transactivation"
<p>This record contains raw data related to the article "Reduction of Cardiac Fibrosis by Interference With YAP-Dependent Transactivation".</p> <p>Abstract</p> <p><strong>Background: </strong>Conversion of cardiac stromal cells into myofibroblasts is typically associated with hypoxia conditions, metabolic insults, and/or inflammation, all of which are predisposing factors to cardiac fibrosis and heart failure. We hypothesized that this conversion could be also mediated by response of these cells to mechanical cues through activation of the Hippo transcriptional pathway. The objective of the present study was to assess the role of cellular/nuclear straining forces acting in myofibroblast differentiation of cardiac stromal cells under the control of YAP (yes-associated protein) transcription factor and to validate this finding using a pharmacological agent that interferes with the interactions of the YAP/TAZ (transcriptional coactivator with PDZ-binding motif) complex with their cognate transcription factors TEADs (TEA domain transcription factors), under high-strain and profibrotic stimulation.</p> <p><strong>Methods: </strong>We employed high content imaging, 2-dimensional/3-dimensional culture, atomic force microscopy mapping, and molecular methods to prove the role of cell/nuclear straining in YAP-dependent fibrotic programming in a mouse model of ischemia-dependent cardiac fibrosis and in human-derived primitive cardiac stromal cells. We also tested treatment of cells with Verteporfin, a drug known to prevent the association of the YAP/TAZ complex with their cognate transcription factors TEADs.</p> <p><strong>Results: </strong>Our experiments suggested that pharmacologically targeting the YAP-dependent pathway overrides the profibrotic activation of cardiac stromal cells by mechanical cues in vitro, and that this occurs even in the presence of profibrotic signaling mediated by TGF-β1 (transforming growth factor beta-1). In vivo administration of Verteporfin in mice with permanent cardiac ischemia reduced significantly fibrosis and morphometric remodeling but did not improve cardiac performance.</p> <p><strong>Conclusions: </strong>Our study indicates that preventing molecular translation of mechanical cues in cardiac stromal cells reduces the impact of cardiac maladaptive remodeling with a positive effect on fibrosis.</p>
BCAT1 drives cardiac fibrosis by promoting proline synthesis machinery
GEO Series GSE244876. Mus musculus. 2 samples. Type: Expression profiling by high throughput sequencing.
Role of cytokines in cardiac fibrosis and exercise
GEO Series GSE129022. Mus musculus. 16 samples. Type: Protein profiling by protein array.
Role of CDCP1 and Cardiac Fibrosis in a Mouse Model of Dilated Cardiomyopathy (DCM)
GEO Series GSE303631. Mus musculus. 4 samples. Type: Other.
Dataset related to the article "A deep-learning approach for myocardial fibrosis detection in early contrast-enhanced cardiac CT images"
<p>This record contains raw data related to the article "A deep-learning approach for myocardial fibrosis detection in early contrast-enhanced cardiac CT images"</p> <p><strong>Aims:</strong> Diagnosis of myocardial fibrosis is commonly performed with late gadolinium contrast-enhanced (CE) cardiac magnetic resonance (CMR), which might be contraindicated or unavailable. Coronary computed tomography (CCT) is emerging as an alternative to CMR. We sought to evaluate whether a deep learning (DL) model could allow identification of myocardial fibrosis from routine early CE-CCT images.</p> <p><strong>Methods and results:</strong> Fifty consecutive patients with known left ventricular (LV) dysfunction (LVD) underwent both CE-CMR and (early and late) CE-CCT. According to the CE-CMR patterns, patients were classified as ischemic (<em>n</em> =&thinsp;15, 30%) or non-ischemic (<em>n</em> =&thinsp;35, 70%) LVD. Delayed enhancement regions were manually traced on late CE-CCT using CE-CMR as reference. On early CE-CCT images, the myocardial sectors were extracted according to AHA 16-segment model and labeled as with scar or not, based on the late CE-CCT manual tracing. A DL model was developed to classify each segment. A total of 44,187 LV segments were analyzed, resulting in accuracy of 71% and area under the ROC curve of 76% (95% CI: 72%−81%), while, with the bull’s eye segmental comparison of CE-CMR and respective early CE-CCT findings, an 89% agreement was achieved.</p> <p><strong>Conclusions:</strong> DL on early CE-CCT acquisition may allow detection of LV sectors affected with myocardial fibrosis, thus without additional contrast-agent administration or radiational dose. Such tool might reduce the user interaction and visual inspection with benefit in both efforts and time.</p>
Cardiac fibrosis
GEO Series GSE253551. Homo sapiens; Mus musculus. 26 samples. Type: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
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DANDI Archive for NWB datasets
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International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.