Cardiac Fibrosis and Remodeling

This study shows that IL11 expression in cardiomyocytes causes cardiac fibrosis, inflammation, and dysfunction, contradicting previous reports of its anti-fibrotic effects.

This study uses a Drosophila model to show that high fat diets alter cardiac ECM morphology and function, with genotype-specific responses to dietary fat.

This study identifies maresin-2's role in modulating ULK1 O-GlcNAcylation to enhance autophagy and improve post-myocardial infarction remodeling.

The paper uses machine learning to analyze myocardial T1 time in UK Biobank data, identifying genetic loci and pathways associated with interstitial fibrosis and related cardiovascular diseases.

This study shows that inhibiting HuR reduces cardiac remodeling after ischemia-reperfusion injury by dampening inflammatory gene expression and immune response, but not initial infarct size.

The paper identifies BRD4-dependent immune-fibroblast crosstalk via IL1B in heart failure, showing IL1B inhibition reduces fibroblast activation and improves cardiac function.

This study shows that HuR-dependent Wisp1 expression is necessary for TGFβ-induced cardiac myofibroblast activity, as HuR inhibition reduces ECM remodeling and contractile functions.

This study shows metformin reduces DDR2-mediated fibrosis in vascular fibroblasts under hyperglycaemia by inhibiting TGF-β1/Smad2/3 signalling.

This study investigates how cardiac fibroblasts respond to hemodynamic changes, identifying Selenbp1 as a key regulator of fibroblast differentiation and collagen turnover in cardiac fibrosis.

This study uses deep learning models and single-cell RNA-seq data to identify molecular targets and signaling pathways involved in macrophage-fibroblast-cardiomyocyte interactions in heart failure.

This study shows that Trpm4 knockout in mice increases cardiac inflammation and fibrosis after myocardial infarction without improving survival.

This paper develops a canine model of chronic ischemic heart failure by ligating different coronary artery branches to study survival and HF progression.

The paper defines the cellular and transcriptional features of cardiac recovery using snRNA-seq, identifying RUNX1 downregulation as a key predictor and potential therapeutic target.

This paper shows that MKK6 deficiency leads to cardiac dysfunction through hyperactivation of the MKK3-p38γ/δ-mTOR pathway, causing hypertrophy and fibrosis, and highlights potential cardiotoxicity of p38 inhibitors.

This study shows TET2 regulates cardiac remodeling by inhibiting endothelial-to-mesenchymal transition, with vitamin C partially improving cardiac function.

The paper predicts mechano-adaptive therapies for myocardial infarction by modeling fibroblast mechanotransduction and identifying 13 drug targets that modulate matrix accumulation in specific regions.

This study investigates how M2-like macrophages regulate post-MI fibrosis through Nrg1/ErbB signaling, showing it suppresses fibroblast senescence and apoptosis.

This study shows that NRK-2 protects against pressure overload-induced cardiac remodeling by inhibiting JNK pathway activation and mitochondrial dysfunction in mice.

The paper uses Google matrix analysis of MetaCore network to predict protein-protein interactions involved in cardiac fibrosis in mouse and human tissues.

This study identifies DDR2-mediated fibronectin regulation as a key mechanism for Angiotensin II-induced AT1R expression in cardiac fibroblasts through Integrin-β1 signaling.

The paper identifies a reversible transcriptional switch in cardiac fibroblasts that governs fibroblast plasticity and contributes to chronic heart disease, with MEOX1 as a key regulator.

This study shows that EC-SOD overexpression reduces cardiac fibrosis and RASSF1A methylation in hypoxic mice.

This study shows that cardiovascular disease risk factors alter the transcriptome of cardiac endothelial cells, promoting mesenchymal features and senescence, with SERPINH1/HSP47 as a potential therapeutic target.

This study examines chromatin accessibility and gene expression in cardiac fibroblasts before and after myocardial infarction using ATAC-seq and RNA-seq, revealing correlations between promoter accessibility and gene expression, and identifying potential transcription factors involved in differential gene expression.

This study identifies GSK-3α in cardiac fibroblasts as a mediator of myocardial fibrosis through the IL-11 and ERK pathway, showing its role in fibroblast activation and cardiac function improvement upon deletion.

The paper examines the epigenetic regulation and expression of five fibrosis-related genes in cardiac fibrosis, identifying super-enhancers and enhancer chromatin features associated with their expression.

This study investigates how matrine reduces isoproterenol-induced myocardial hypertrophy in rats by modulating the Akt/mTOR/p70S6K/eIF4E signaling pathway.

This study shows that IL-35 pretreatment reduces LPS-induced heart injury by decreasing inflammation, apoptosis, and fibrosis through inhibiting NF-κBp65 and TGF-β1/Smad2/3 pathways.

This study identifies DDR2-dependent SRF activation as a mechanism regulating cell survival and cell cycle progression in cardiac fibroblasts through ERK1/2 MAPK signaling.