Cardiac Fibrosis and Remodeling

Interleukin 11-induced microRNAs as functional mediators and circulating biomarkers of cardiac fibrosis

This study identifies miRNA-27b-5p and miRNA-497-5p as downstream effectors of IL-11-induced cardiac fibrosis and potential circulating biomarkers in aortic stenosis.

Red yeast rice-derived MKA ameliorates cardiac hypertrophy in hypertensive rats by inhibiting ERK1/2/c-Fos pathway

This study shows that MKA from red yeast rice reduces cardiac hypertrophy in hypertensive rats by inhibiting the ERK1/2/c-Fos pathway, with no organ toxicity and transgenerational benefits.

Immune Transcriptional Signatures Across Human Cardiomyopathy Subtypes: A Multi-Cohort Integrative Computational Analysis

This study identifies an immune-fibrotic transcriptional signature across cardiomyopathy subtypes using multi-cohort transcriptomic analysis and develops a nine-gene biomarker panel.

Inhibition of Gasdermin D by Disulfiram Attenuates Cardiac Inflammation and Fibrosis following Ischaemia Reperfusion Injury

This paper shows that Disulfiram reduces cardiac inflammation and fibrosis after heart attack by inhibiting the GSDMD pathway.

Minimally invasive myocardial infarction model recapitulates patient immune responses and reveals a pathogenic role for immature neutrophils

This study compares two myocardial infarction models, showing the intact-chest model better reflects human immune responses and identifies immature neutrophils as contributors to cardiac dysfunction.

Lipoxins Regulate Intercalated Disk-Associated Signaling and Immune Remodeling in Dilated Cardiomyopathy

This study shows lipoxins modulate immune responses and cardiac signaling in male MLPko mice with dilated cardiomyopathy, but not in females.

Macrophage SLC9A1 Links Endocytic Trafficking to Innate Immune Activation in Myocardial Injury

This study identifies SLC9A1 as a mediator linking macrophage endocytic trafficking to innate immune activation in myocardial injury, showing its role in inflammation and cardiac remodeling.

Genetic Deletion of ASIC3 Alters Left Ventricular Remodeling and Autonomic Function After Myocardial Infarction in Mice

This study shows that genetic deletion of ASIC3 reduces left ventricular dilation and improves autonomic function after myocardial infarction in mice.

Targeting immunometabolic pathways with AZD1656 alleviates inflammation and metabolic dysfunction in type 2 diabetic cardiomyopathy

In db/db mice, six weeks of AZD1656 improved diastolic function, cardiac metabolism and infarct size, with increased Treg infiltration and less fibrosis, without glycaemic change.

PARP6-dependent vimentin ADP-ribosylation prevents myofibroblast activation in cardiac fibrosis

WISP1 drives a mechanically active immune modulatory and proliferative cardiac myofibroblast state

This study shows WISP1 drives a unique proliferative and immune-modulatory myofibroblast state in cardiac fibroblasts, acting through a non-canonical P38 MAPK pathway.

Regulation of the Balance between Concentric and Eccentric Cardiac Hypertrophy by a CDC14A-KMT5A Signaling Pathway

This paper identifies CDC14A and KMT5A as regulators of concentric vs. eccentric cardiac remodeling through epigenomic control of gene transcription, with CDC14A as a potential therapeutic target for heart failure.

Targeting Galectin-3 C-epitope oligomers associated maladaptive mechanotransductive signaling in pressure-overload induced left ventricular cardiac hypertrophy

This study identifies Gal-3 C-epitope oligomers as pathogenic in cardiac hypertrophy and shows that Amalaki Rasayana and gallic acid reduce their levels and mitigate adverse effects.

Genetic Determinants of Heart Failure Susceptibility and Response in the Collaborative Cross Mouse Population

The paper identifies genetic loci associated with heart failure susceptibility and response in mice, highlighting candidate genes that modulate cardiac hypertrophy.

Elevated IL-1 beta plasma levels, altered platelet activation and cardiac remodeling lead to moderately decreased LV function in Alzheimer transgenic mice after myocardial ischemia and reperfusion

This study shows that Alzheimer's transgenic mice experience reduced left ventricular function after myocardial ischemia and reperfusion, linked to elevated IL-1 beta, altered platelet activation, and cardiac remodeling.

Neutrophil terminal programming in the ischemic heart drives fibrosis after myocardial infarction

This study shows that neutrophils in the ischemic heart undergo terminal programming to drive fibrosis after myocardial infarction.

Multiomics reveals epigenetic control of fibroblast activity after myocardial infarction and a key role for RUNX transcription factors

This study uses multi-omics approaches to show that Runx1 regulates cardiac fibroblast activity and differentiation after myocardial infarction, with its deletion improving cardiac repair.

Multicellular signaling and partial recovery define reverse cardiac remodeling

This study shows that reverse cardiac remodeling is a constrained multicellular state with partial recovery of metabolic programs but persistent inflammatory-mitochondrial dysfunction, mediated by lymphatic-derived Reelin.

Drp1-mediated mitochondrial fission protects macrophages from mtDNA/ZBP1-mediated sterile inflammation and inhibits post-infarct cardiac remodeling

This study shows that Drp1 in macrophages prevents mtDNA release and inflammation, reducing cardiac remodeling after heart attack.

High burden of premature ventricular contractions upregulates transcriptional markers of inflammation and promotes adverse cardiac remodeling linked to cardiomyopathy

This study shows that high PVC burden causes inflammation and fibrosis, leading to adverse cardiac remodeling and increased risk of heart failure and sudden cardiac death.

Pharmacological inhibition of 11βhydroxysteroid dehydrogenase type 1 after myocardial infarction targets extracellular matrix processing and preserves cardiac function in a translational mini-pig model

This study shows that inhibiting 11βHSD1 after myocardial infarction preserves cardiac function and prevents adverse remodelling in a mini-pig model.

Short-term but not long-term triiodothyronine treatment improved cardiac function after myocardial infarction in male wild-type mice

This study shows short-term T3 treatment improves cardiac function after MI in WT mice, while long-term T3 causes hypertrophy without functional benefit and may worsen function in TR-deficient mice.

SMOC1 Regulates Endothelial-to-Mesenchymal Transition During Cardiac Repair After Myocardial Infarction

This study identifies SMOC1 as a regulator of EndMT in cardiac repair, showing its role in modulating TGF-β/endoglin signaling and preventing pathological fibrosis after MI.

Modeling the Interplay of Sex Hormones in Cardiac Hypertrophic Signaling

The paper develops a logic-based systems biology model of cardiac hypertrophy incorporating sex hormones and validates it to show testosterone has a greater impact on hypertrophy than estradiol.

AI-based Predictive Signaling Pathway Profiling in Cardiac Fibrosis Suggests a Novel Combinatorial Treatment Strategy

The paper uses AI to analyze signaling pathways in cardiac fibrosis, identifying a dual-target treatment strategy with timed inhibition of JAK-STAT and TGF-β to reduce fibrosis without impairing acute scar formation.

PARP1 deficiency induces aging-associated cardiac failure via activation of Akt signalling

This study shows PARP1 deficiency causes aging-related cardiac failure by activating Akt signaling, leading to hypertrophy and fibrosis in mice.

Haematopoietic loss of KDM6A impairs cardiac recovery in heartfailure via epigenetic reprogramming of myeloid cells

This study shows that loss of KDM6A in hematopoietic cells impairs cardiac recovery after heart failure by causing epigenetic changes in myeloid cells that increase inflammation and worsen cardiac outcomes.

Identification of epigenetic regulators of fibrotic transformation in cardiac fibroblasts through bulk and single-cell CRISPR screens

The paper identifies epigenetic regulators of fibrotic transformation in cardiac fibroblasts using bulk and single-cell CRISPR screens and shows KAT5 inhibition reduces fibrotic responses in human fibroblasts.

Regional and Temporal Changes in Early Structural Remodeling Following Myocardial Infarction via Semi-Automatic Image Analysis

This study uses semi-automatic image analysis to show late reperfusion therapy reduces infarct border size and accelerates healing phases in rat myocardium.

Nuclear GAPDH cascade mediates stress-dependent pathological cardiac growth

This study identifies nuclear GAPDH translocation as a mediator of stress-induced cardiac hypertrophy through BRG1-associated chromatin remodeling in mice and human patients.