Cardiac Fibrosis and Remodeling

T cell-derived IFNγ instructs ECM crosslinking by cardiac fibroblasts through LOXL3 in experimental cardiometabolic HFpEF

This study identifies T cell-derived IFNγ as a driver of ECM stiffening in HFpEF via LOXL3 in cardiac fibroblasts, showing therapeutic potential for targeting this pathway.

PKNs are required for cardiac hypertrophy induced by angiotensin II in mice

The paper investigates the role of PKN isoforms in cardiac hypertrophy induced by angiotensin II in mice, finding that Pkn1/3 are required for sustained hypertrophy while Pkn2 does not substitute for them.

Cardiac Hemorrhage Precedes Hypertension-induced Fibrosis inPlasminogen Activator Inhibitor-1 Deficient Mice

This study shows that PAI-1 deficiency leads to early cardiac hemorrhage and fibrosis under hemodynamic stress, with mutations in the protease-inhibitory domain causing similar pathology.

The epidermal growth factor (EGF) receptor family network in cardiac hypertrophy and heart failure

EGFR-family ligand mRNAs shift in failing human hearts; NRG1 and EGF drive distinct, differently ERBB2-dependent transcriptional programmes in rat cardiomyocytes; afatinib blunts mouse angiotensin II hypertrophy but worsens fibrosis.

Interpretable computational SHG microscopy enables quantitative tissue phenotyping of cardiac remodeling in nonischemic heart failure

The paper develops an interpretable computational SHG microscopy framework to classify cardiac remodeling states in mice with high accuracy.

Enzymatic extracellular matrix remodeling in ex vivo slices of aged myocardium

This study shows enzymatic remodeling of aged cardiac ECM reduces stiffness but preserves contractility and some age-related transcriptional features in ex vivo myocardial slices.

A Compact Regulatory Logic Governs Fibroblast Cell State Plasticity in Fibrosis

The paper identifies a compact regulatory logic governing fibroblast plasticity in fibrosis by analyzing enhancer repression and gene perturbations across multiple tissues.

Sex chromosome and gonadal regulation of cardiac myofibroblast activation decoupled using mechanically tunable hydrogels and the Four Core Genotypes model

This study decouples the effects of sex chromosomes and gonadal sex on cardiac myofibroblast activation using FCG mice and hydrogel cultures, revealing sex-specific gene and protein expression patterns.

Small GTPases RhoA and RhoC coordinately regulate cardiomyocyte size in the mouse heart

This study shows RhoA and RhoC regulate cardiomyocyte size and cardiac remodeling, with compensatory effects and stress-dependent contributions to hypertrophy and function.

Cardiometabolic stress induces atrial myopathy in mice, characterized by structural remodelling, metabolic dysfunction, and incomplete transcriptional recovery.

This study shows that cardiometabolic stress causes atrial myopathy in mice, with partial recovery of metabolic and transcriptional changes after stress removal.

Targeting Cardiac Fibrosis with Chimeric Antigen Receptor Neutrophils Derived from Human Pluripotent Stem Cells

This study develops hPSC-derived FAP CAR neutrophils to target cardiac fibrosis, showing in vitro cytotoxicity and improved left ventricular ejection fraction in a mouse MI model.

Spatial organization of fibroblast subpopulations and niches across acute repair and chronic fibrotic remodeling of the human myocardium

This study identifies spatially distinct fibroblast subpopulations and niches in human myocardial fibrosis across different disease states and their associations with fibrotic remodeling and cardiac dysfunction.

IL27 exerts a powerful effect on systolic overload-induced cardiac inflammation, fibrosis, and heart failure development

This study shows IL-27 promotes cardiac inflammation, fibrosis, and heart failure in mice by modulating immune and non-immune cells, suggesting it as a therapeutic target.

A tRNA-derived small RNA orchestrates cardioprotection through distinct cell-type-specific mechanisms

This study identifies a tRNA-derived small RNA that reduces cardiac fibrosis and hypertrophy through cell-type-specific mechanisms in mouse and human cardiac cells.

Calcium dysregulation amplifies fibrotic responses to TGFβ in human Friedreich's ataxia fibroblasts

This study shows that calcium dysregulation in Friedreich's ataxia fibroblasts enhances fibrotic responses to TGFβ by affecting NFAT-controlled genes and NCX1 function.

IL-17A Mediates Cardiac Hypertrophy in Chronic Kidney Disease through the IL-23/Th17 Axis.

This study shows that IL-17A promotes cardiac hypertrophy in CKD via the IL-23/Th17 axis, with IL-12p40 as a potential biomarker and therapeutic target.

Spatial transcriptomics reveals selective vulnerability of cardiac neural crest-derived glial cells in human myocardial infarction

The paper uses spatial transcriptomics to show that cardiac neural crest-derived glial cells are selectively lost in myocardial infarction, with metabolic failure and pyroptosis implicated as mechanisms.

Collateral Immune Cell Signaling Compromises the Efficacy of T-cell Engaging Therapies for Cardiac Fibrosis

This study shows that FAP-targeted BiTE(R) molecules, intended to reduce cardiac fibrosis, instead worsen heart function by triggering harmful immune responses.

Microtubule-associated protein 1S (MAP1S): a cardioprotective factor against post-myocardial infarction remodeling via apoptosis inhibition

This study shows that MAP1S protects the heart from post-MI apoptosis and remodeling by modulating the Hippo pathway in mice and cultured cardiomyocytes.

Cardiomyocyte-specific loss of Smyd5 leads to a robust activation of inflammatory signaling and heart failure in mice.

This study shows that loss of Smyd5 in cardiomyocytes causes inflammation and heart failure in mice by reducing H4K20me3 and increasing Il-6 expression.

Complementary Models of Cardiometabolic Stress Reveal Conserved Molecular Programs Driving Cardiac Remodeling

The paper identifies conserved molecular responses to cardiometabolic stress across different disease models and finds PAI-1 as a key mediator of cardiac remodeling.

Identification of osteopontin as a positional and functional candidate gene for cardiac hypertrophy in the SHRSP rat

The paper identifies osteopontin (Spp1) as a positional and functional candidate gene for cardiac hypertrophy in SHRSP rats through congenic strain analysis and transcriptome profiling.

4-Hydroxybenzaldehyde Attenuates Isoproterenol-induced Cardiac Fibrosis via TGF-β-Smad2/3 Signaling Pathway

This study shows that 4-HBA reduces cardiac fibrosis by inhibiting the TGF-β/Smad2/3 pathway in both in vivo and in vitro models.

Mitral regurgitation induces a unique fibroblast population associated with atrial fibrillation susceptibility

This study identifies a unique fibroblast population in MR-induced atrial fibrosis that correlates with AF susceptibility in a canine model.

Dysferlin is a novel regulator of COMP-positive matrifibrocytes in heart failure

This study identifies dysferlin as an antifibrotic regulator that limits fibroblast differentiation and myocardial fibrosis in heart failure.

Lanifibranor (IVA-337) - a pan-PPAR agonist suppresses TGF-β1-induced cardiac fibrosis and rescues cardiomyocyte function

This study shows lanifibranor reduces TGF-β1-induced cardiac fibrosis and improves cardiomyocyte function in human models.

TREM2 drives accumulation of pro-scarring monocyte-derived macrophages in the infarcted myocardium

This study shows TREM2 drives pro-scarring macrophage accumulation in infarcted myocardium, leading to fibrosis and reduced cardiac repair.

The dual PPAR-α/δ agonist elafibranor attenuates TGF-β1-induced cardiac fibrosis through redox-metabolic and bioenergetic reprogramming in human cardiac models

This paper shows that elafibranor reduces TGF-β1-induced cardiac fibrosis by improving redox-metabolic and bioenergetic processes in human cardiac models.

Comparison of Culture Systems for Mouse Living Myocardial Slices in Cardiac Fibrosis Research

This study compares two culture systems for mouse living myocardial slices, finding the biomimetic system provides better viability, structure, and function for cardiac fibrosis research.

Myeloid cell recruitment propels right ventricular dysfunction in HFpEF via sterile inflammation.

This paper shows that myeloid cell recruitment drives right ventricular dysfunction in HFpEF through sterile inflammation in both mice and humans.