Cardiac Fibrosis and Remodeling

Galectin-3 C-epitope, ANP, PPIA, and albumin function as drug-responsive panel biomarkers and therapeutic targets in aging and pressure overload-induced cardiac hypertrophy

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.

Macrophages Lacking TSC2 have mTORC1-dependent GPNMB Augmentation Ameliorating Cardiac Ischemia-Reperfusion Injury

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.

CD163+/Dab2+ Macrophages Alleviate Cardiac Hypertrophy via Nrg2/ErbB4-Mediated Mitochondrial Reprogramming

Adropin protects against cardiac remodeling and metabolic dysfunction in a mouse model of HFpEF

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.

STAT3 expression is reduced in cardiac pericytes in HFpEF and its loss reduces cellular adhesion and induces pericyte senescence

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

Defining the cardiac fibroblast secretome in the healthy and infarcted mouse heart

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

Titin cleavage is a driver of cardiomyocyte disengagement and reactive myocardial fibrosis

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

Contributions of mechanical loading and hormonal changes to eccentric hypertrophy during volume overload: a Bayesian analysis using logic-based network models.

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.

An inducible genetic model of chronic hypoxic signaling in cardiomyocytes precipitates severe cardiomyopathy and remodeling.

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.

SNRK regulates TGFbeta levels in atria to control cardiac fibrosis

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

Bone marrow mesenchymal stromal cells mediate cellular inflammation in HFpEF

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.

UNCONVENTIONAL INTERLEUKIN-1 SIGNALING IN CARDIAC DYSFUNCTION

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.

Logic-based machine learning predicts how escitalopram attenuates cardiomyocyte hypertrophy

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

Inhibition of Atrial Natriuretic Peptide Clearance Reduces Myocardial Fibrosis and Improves Cardiac Function in Diabetic Rats

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.

Expression of the Close homolog of L-1 and embigin identifies activated myofibroblasts.

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.

Circuit to target approach defines an autocrine myofibroblast loop that drives cardiac fibrosis

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

Endothelial decorin is increased by ageing and, induces inflammation and diastolic dysfunction in the heart

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.

Dietary Branched Chain Amino Acids Modify Post-Infarct Cardiac Remodeling and Function in the Murine Heart

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.

A cross-species multimodal database of gene expression in cardiac hypertrophy

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.

17β-Estradiol Counteracts Pathological Microtubule Remodeling To Enhance Cardiac Function

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

Cardiac fibrosis inhibitor CTPR390 prevents structural and morphological changes in collagen and fibroblasts of engineered human connective tissue

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

LSD1 demethylase inhibition prevents cardiac fibrosis in both ischemic and congenital diseases in mice and pig models

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.

Unravelling the molecular activation of the reparative cardiac fibroblasts after myocardial infarction

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

Sex-specific regulation of the cardiac transcriptome by the protein phosphatase 2A regulatory subunit B55α

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

Fibroblast-specific protein-protein interactions for myocardial fibrosis from MetaCore network

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

Female Specific Restrictive Cardiomyopathy and Metabolic Dysregulation in transgenic mice expressing a Peptide of the Amino-Terminus of GRK2

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.

Rapid onset fibrotic remodeling and ventricular dysfunction induced by phenylephrine involve targeted reprogramming of myocyte and fibroblast transcriptomes

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

Novel fluorescence-based methods to determine infarct and scar size in murine models of reperfused myocardial infarction

The paper compares fluorescence staining methods to classical histochemical techniques for determining infarct and scar size in murine reperfused myocardial infarction models.

METTL3 Modulates Radiation-Induced Cardiac Fibrosis via the Akt/mTOR Pathway

This study investigates how METTL3 contributes to radiation-induced cardiac fibrosis by activating the Akt/mTOR pathway, showing that METTL3 overexpression worsens fibrosis while its knockdown reduces it.

When the liver is in poor condition, so is the heart - cardiac remodelling in MASH mouse models

This study examines cardiac remodelling in MASH mouse models, finding adverse structural changes in the heart linked to liver disease, not overfeeding or aging.