Ontology highlight
ABSTRACT:
PROVIDER: PRJNA824544 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Here, we performed pathological cardiac hypertrophy transcriptome analyses by using heart tissue from Sham or TAC surgery to identify the charecteric in pathological cardiac hypertrophy. In addition, through combined analysis with the aging-associated transcriptome to identify the similarity and difference between heart ageing and pathological cardiac hypertrophy.
2025-01-29 | GSE203083 | GEO
Project description:Gene profiling of pathological cardiac hypertrophy vs physiological hypertrophy
| PRJNA100305 | ENA
Project description:miRNA-99 family diverges physiological cardiac hypertrophy to pathological cardiac hypertrophy
| PRJNA297403 | ENA
Project description:Aim: The heart undergoes pathological remodelling under increased stress and neuronal imbalance. MicroRNAs (miRNAs) are involved in post-transcriptional regulation of genes in cardiac physiology and pathology. However, the mechanisms underlying miRNA-mediated regulation of pathological cardiac remodelling remain to be studied. This study aims to explore the function of endogenous microRNA-27b-3p (miR-27b-3p) in pathological cardiac remodelling. Methods and results: We found that miR-27b-3p expression was elevated in heart of patients with cardiac hypertrophy and in transverse aortic constriction (TAC)-induced cardiac hypertrophy mouse model. MiR-27b-3p-knockout mice showed significantly attenuated cardiac hypertrophy, fibrosis, and inflammation induced by two independent pathological cardiac hypertrophy models, TAC and Angiotensin II (Ang II) perfusion. Transcriptome sequencing analysis revealed that miR-27b-3p deletion significantly downregulated TAC-induced cardiac hypertrophy, fibrosis, and inflammatory genes. We identified fibroblast growth factor 1 (FGF1) as a novel miR-27b-3p target gene in the heart, which was upregulated in miR-27b-3p-null mice. Conclusions: Our study has demonstrated that miR-27b-3p induces pathological cardiac remodelling and suggests that inhibition of endogenous miR-27b-3p or administration of FGF1 might have the potential to suppress cardiac remodelling in a clinical setting.
2022-07-27 | GSE158191 | GEO
Project description:Cardiac hypertrophy is an adaptive response to pressure overload aimed at maintaining cardiac function. However, prolonged hypertrophy significantly increases the risk of maladaptive cardiac remodeling and heart failure. The role of cardiac long non-coding RNAs in cardiac hypertrophy and cardiomyopathy is not well understood. lincRNA-p21 was induced in mouse and human cardiomyopathy tissue. Global and cardiac-specific lincRNA-p21 knockout significantly suppressed pressure overload-induced ventricular wall thickening, stress marker elevation, and deterioration of cardiac function. Genome-wide transcriptome analysis and transcriptional network analysis revealed that lincRNA-p21 acts in trans to stimulate the NFAT/MEF2 pathway. Mechanistically, lincRNA-p21 bound to the scaffold protein KAP1. lincRNA-p21 cardiac-specific knockout suppressed stress-induced nuclear accumulation of KAP1, and KAP1 knockdown attenuated cardiac hypertrophy and NFAT activation. KAP1 positively regulated pathological hypertrophy by physically interacting with NFATC4 to promote the overactive status of NFAT/MEF2 signaling. Importantly, GapmeR ASO depletion of lincRNA-p21 similarly inhibited cardiac hypertrophy and adverse remodeling, highlighting the therapeutic potential of inhibiting lincRNA-p21.
2024-06-11 | GSE262936 | GEO
Project description:Purpose: The physiological cardiac hypertrophy is an adaptive condition that does not associate with myocyte cell death while pathological hypertrophy is a maladaptive condition associated with myocyte cell death. Alpha-2 macroglobulin (α-2M) an acute phase protein induces cardiac hypertrophy via the ERK1,2 and PI3K/Akt signaling. This study is aimed at exploring the miRNome of α-2M induced hypertrophied cardiomyocytes and to understand the role of miRNAs in determination of pathological and physiological hypertrophy. Methods: Hypertrophy was induced in H9c2 cardiomyoblasts using alpha-2 macroglobulin. The induction of hypertrophy is confirmed by microscopy and gene expression studies. Subsequently, the total RNA was isolated and small RNA sequencing was executed in Illumina HiSeq 2000. Results: Analysis of small RNA reads revealed the differential expression of a large set of miRNAs during hypertrophy. Among the differentially expressed candidates, miR-99 family (miR-99a, miR-99b and miR-100) showed significant downregulation upon α-2M treatment while isoproterenol treatment (pathological hypertrophy) upregulated their expression. The binding site for Egr1 transcription factor was identified in the promoter region of miR-99 family, and interestingly all miRNAs with Egr1 binding site proven by ChIP-Seq were downregulated during physiological hypertrophy Conclusions: The results proved Egr-1 mediated regulation of miR-99 family determines the uniqueness of pathological and physiological hypertrophy. Upregulated miR-99 expression during pathological hypertrophy suggests that it can be a valuable diagnostic marker and potential therapeutic target for cardiac hypertrophy and heart failure. Small RNA profiles of control and hypertrophied cardiomyocyte H9c2 cells were generated by deep sequencing using Illumina HiSeq 2000
2015-11-01 | E-GEOD-73597 | biostudies-arrayexpress
Project description:We show that Bmx-deficiency reduces angiotensin II -induced cardiac hypertrophy and pathological gene expression Angiotensin II or NaCl were infuced for two weeks into wild-type and Bmx-deficient mice to induce cardiac hypertrophy
2013-11-30 | E-GEOD-47420 | biostudies-arrayexpress
Project description:Cardiovascular disease remains the leading cause of mortality globally. While cardiac hypertrophy initially arises as a compensatory adaptation of cardiomyocytes to stress, physiological and pathological cardiac hypertrophy exhibit distinct underlying mechanisms and prognoses. However, the precise mechanisms by which cardiomyocytes differentially respond to various stimuli, resulting in distinct forms of hypertrophy thereby ultimately determining divergent cell fates, remain unclear. Here, we demonstrate that metabolic flexibility governs cardiomyocyte fate during cardiac hypertrophy and identified that this metabolic governance is mediated through YTHDF1-dependent RNA epigenetic regulation. In vivo, cardiomyocyte-specific YTHDF1 deficiency leads to maladaptive cardiac remodeling in response to swimming exercise and additionally exacerbates pathological cardiac remodeling under pressure overload stimulation. In vitro, YTHDF1 functions as a switch to regulate the type of cardiomyocyte hypertrophy in a RNA m6A-dependent manner. The YTHDF1/KLF11/HIF1α axis controls cardiomyocyte fate during hypertrophy via balancing metabolic flexibility to meet energy demands. Cardiac-specific overexpression of YTHDF1 alleviates pathological cardiac remodeling. Our findings reveal a previously unrecognized regulatory pathway wherein YTHDF1 serves as a sensor responding to diverse stresses and controling cardiomyocyte fate during hypertrophy via the YTHDF1/KLF11/Hif1α axis. These results highlight a novel therapeutic approach that may inform the development of exercise intervention strategies, suggesting that enhancing oxidative metabolism may serve as a potential treatment option for cardiac diseases.
2026-08-15 | GSE300276 | GEO
Project description:The heart grows in response to pathological and physiological stimuli, while the former often precedes cardiomyocyte loss and heart failure, the latter paradoxically protects the heart and enhances cardiomyogenesis. Long noncoding RNAs (lncRNAs) are important in cardiac development and disease, less is known about their roles in physiological hypertrophy or cardiomyogenesis. The purpose of this study was to compare transcriptome profilings in exercise-induced physiological cardiac growth and stress-induced pathological cardiac growth. We identified a set of lncRNAs called long noncoding exercise associated cardiac transcripts (lncExACT). One of them, lncExACT1, whose cardiac expression was downregulated after exercise but upregulated after transverse aortic constriction. Inhibition of lncExACT1 induced physiolgoical cardiac growth while overexpression of lncExACT1 induced pathological hypertrophy and heart failure.
2022-10-18 | GSE186081 | GEO
Project description:Purpose: The physiological cardiac hypertrophy is an adaptive condition that does not associate with myocyte cell death while pathological hypertrophy is a maladaptive condition associated with myocyte cell death. Alpha-2 macroglobulin (α-2M) an acute phase protein induces cardiac hypertrophy via the ERK1,2 and PI3K/Akt signaling. This study is aimed at exploring the miRNome of α-2M induced hypertrophied cardiomyocytes and to understand the role of miRNAs in determination of pathological and physiological hypertrophy. Methods: Hypertrophy was induced in H9c2 cardiomyoblasts using alpha-2 macroglobulin. The induction of hypertrophy is confirmed by microscopy and gene expression studies. Subsequently, the total RNA was isolated and small RNA sequencing was executed in Illumina HiSeq 2000. Results: Analysis of small RNA reads revealed the differential expression of a large set of miRNAs during hypertrophy. Among the differentially expressed candidates, miR-99 family (miR-99a, miR-99b and miR-100) showed significant downregulation upon α-2M treatment while isoproterenol treatment (pathological hypertrophy) upregulated their expression. The binding site for Egr1 transcription factor was identified in the promoter region of miR-99 family, and interestingly all miRNAs with Egr1 binding site proven by ChIP-Seq were downregulated during physiological hypertrophy Conclusions: The results proved Egr-1 mediated regulation of miR-99 family determines the uniqueness of pathological and physiological hypertrophy. Upregulated miR-99 expression during pathological hypertrophy suggests that it can be a valuable diagnostic marker and potential therapeutic target for cardiac hypertrophy and heart failure.
2015-11-01 | GSE73597 | GEO