Cardiac Fibrosis and Remodeling

This study identifies isoliensinine's role in improving cardiac function by enhancing COX6A2 expression through swimming exercise, revealing a novel signaling axis in pathological cardiac hypertrophy.

This study shows adiponectin receptor agonism prevents right ventricular fibrosis and inflammation in a mouse model of Duchenne muscular dystrophy.

The paper identifies a biomarker panel responsive to treatment in cardiac hypertrophy and aging, showing that galectin-3 C-epitope, ANP, PPIA, and albumin levels decrease with therapeutic intervention in rat models and human patients.

This study shows that macrophages with constitutive mTORC1 activation via TSC2 deletion reduce inflammation and improve cardiac function after ischemia-reperfusion injury by increasing GPNMB expression.

This study shows Adropin treatment reverses cardiac dysfunction and metabolic defects in a mouse model of HFpEF by reducing O-GlcNAcylation of LCAD and improving fatty acid oxidation.

The paper identifies reduced STAT3 expression in cardiac pericytes in HFpEF and shows its loss leads to senescence and impaired adhesion.

This study identifies the secretome of cardiac fibroblasts in healthy and infarcted mouse hearts, revealing dynamic paracrine factors and potential biomarkers or therapeutic targets.

This study shows that titin cleavage drives cardiomyocyte disengagement and fibrosis in heart disease, contributing to myocardial remodeling.

This paper uses a Bayesian network model to analyze how mechanical loading and hormonal changes contribute to eccentric hypertrophy in volume overload, showing neurohormonal responses drive growth rather than initial stretch.

This study shows CD40 agonists promote myocardial inflammation by activating CCR2+ macrophages and CD8 T-cells, leading to heart failure.

This paper develops an inducible Vhl knockout mouse model to study chronic hypoxic stress in cardiomyocytes, revealing early gene expression changes linked to cardiac remodeling and disease.

This study shows that SNRK in atrial cardiomyocytes reduces TGFbeta1 levels, preventing fibrosis and heart failure.

The paper shows that bone marrow stromal cells in HFpEF respond to IFNγ, driving monocyte expansion and fibrosis, which can be mitigated by IFNγ receptor deletion.

This study investigates unconventional IL-1β signaling via PI3Kγ in cardiomyocytes, showing kinase-independent mechanisms link IL-1β to cardiac dysfunction and potential heart failure treatment insights.

The paper uses a logic-based machine learning method to predict how escitalopram reduces cardiomyocyte hypertrophy, validated through experiments and patient data.

This study shows that inhibiting atrial natriuretic peptide (ANP) clearance with a mutated peptide (MANP) reduces myocardial fibrosis and improves cardiac function in diabetic rats.

The paper identifies ChL-1 and embigin as novel markers for activated myofibroblasts, showing their expression in fibrotic tissues and their utility for targeting these cells.

The paper models a macrophage-myofibroblast circuit to predict fibrosis types and shows targeting the myofibroblast autocrine loop reduces fibrosis after myocardial infarction.

This study identifies decorin as a factor induced by aging that contributes to cardiac inflammation and diastolic dysfunction through pro-inflammatory effects in the myocardium.

This study shows that a low branched-chain amino acid (BCAA) diet reduces cardiac remodeling and preserves function after myocardial infarction in male mice, with less effect in females.

The paper curates a cross-species multimodal database of gene expression in cardiac hypertrophy and introduces an interactive web tool for exploring gene expression across multiple omics layers.

This study shows 17β-estradiol counteracts pathological microtubule remodeling in cardiomyocytes, improving cardiac function and preventing cellular hypertrophy and structural abnormalities.

This study shows that CTPR390 prevents structural and morphological changes in collagen and fibroblasts in a 3D human cardiac model.

This study shows that LSD1 inhibitors reduce cardiac fibrosis and improve ventricular function in both mouse and pig models of ischemic and congenital heart diseases.

The paper identifies molecular dynamics and a new marker, Aspn, for reparative cardiac fibroblasts in mice, pigs, and patients after myocardial infarction.

This study investigates the role of B55α in cardiac transcriptome regulation, finding sex-specific effects on cardiac fibrosis and gene expression.

The paper identifies fibroblast-specific protein-protein interactions driving myocardial fibrosis using the MetaCore network and proposes a method to reverse fibrotic cascades.

This study shows that female mice with cardiac-restricted GRK2 amino-terminal peptide expression develop restrictive cardiomyopathy and metabolic dysregulation under pressure overload, unlike males.

This study shows that phenylephrine induces rapid fibrotic remodeling and ventricular dysfunction in mice through myocyte and fibroblast transcriptome reprogramming.