Cardiac Fibrosis and Remodeling

Loss of MGST1 during fibroblast differentiation enhances vulnerability to oxidative stress in human heart failure

The paper identifies MGST1 as a key antioxidant gene in cardiac fibroblasts, showing its loss in heart failure increases oxidative stress and ferroptosis susceptibility.

Deciphering human heart failure with preserved ejection fraction (HFpEF) at single cell resolution

This paper uses single-nucleus RNA sequencing to analyze HFpEF myocardium, identifying transcriptional changes in cardiomyocytes, endothelial cells, fibroblasts, and macrophages that suggest metabolic, inflammatory, and fibrotic mechanisms.

A cross-study transcriptional patient map of heart failure defines conserved multicellular coordination in cardiac remodeling

This paper integrates bulk and single-cell transcriptomic data from 25 heart failure studies to identify conserved multicellular coordination patterns in cardiac remodeling.

CD4+ T cells fuel the Duchenne cardiomyopathy

This study shows CD4+ T cells drive cardiomyopathy in Duchenne muscular dystrophy by promoting fibrosis and dysfunction, using Mdx mice and single-cell RNA sequencing.

Low-dose infusion of a superagonistic anti-CD28 monoclonal antibody ameliorates inflammation after acute myocardial infarction in pigs

This study shows low-dose CD28-SA infusion reduces inflammation and promotes wound healing in pigs after myocardial infarction by increasing Treg cells and reducing TNF-producing cells.

skNAC is a Key Driver of Cardiomyocyte Integrity Against Pathological Cardiac Hypertrophy and Heart Failure

This study identifies skNAC as critical for maintaining cardiomyocyte integrity and preventing heart failure by regulating proteome homeostasis and metabolic adaptation during pathological hypertrophy.

Targeting platelet GPVI or GPIIb/IIIa only minimally affect acute inflammation and cardiac repair in experimental permanent myocardial infarction

Deep Learning-Enhanced 3D Imaging Unveils Semaglutide Impact on Cardiac Fibrosis

This paper develops a 3D imaging and deep learning method to quantify cardiac fibrosis in mice and shows semaglutide reduces hypertrophy and perivascular fibrosis but not replacement fibrosis.

Sex-Specific Characterization of a Novel Osteoarthritis-Induced Heart Failure Model in Mice

This study characterizes a novel mouse model of OA-induced heart failure, revealing sex-specific cardiac remodeling and molecular pathways associated with different HF phenotypes.

Vascular niches are the primary hotspots for aging within the multicellular architecture of cardiac tissue

This study identifies vascular niches as key hotspots for age-related inflammation and fibrosis in cardiac tissue using single-nucleus RNA sequencing and spatial transcriptomics.

The Adipomyokine Follistatin-like-1 Restores Cardiovascular Function in a Swine Model of Diabetic Myocardial Infarction

This study shows that subcutaneous administration of ngFSTL1 improves cardiac and vascular function in a swine model of diabetic myocardial infarction.

Adventitial leptin receptor-expressing fibroblasts are preferential contributors to fibrotic remodeling of the heart post infarction

This study identifies adventitial leptin receptor-expressing fibroblasts as key contributors to cardiac fibrosis after myocardial infarction in mice and humans.

Activated fatty acid synthesis pathway in macrophages propagates pathogenic fibroblast expansion after myocardial infarction

This study shows that macrophage fatty acid synthesis promotes fibroblast expansion and fibrosis after myocardial infarction.

Integrated analysis reveals neuro-immune pathway in the central nervous system that supports SGLT2is protective effects in treatment of cardiac remodeling

This study identifies a neuro-immune pathway in the central nervous system that mediates the protective effects of SGLT2 inhibitors on cardiac remodeling using preclinical and clinical data.

Systems analysis reveals neuregulin-1 control of cardiomyocyte size and shape mediated by distinct PI3K and p38 pathways

The paper identifies distinct PI3K and p38 pathways mediating neuregulin-1-induced changes in cardiomyocyte size and shape through systems analysis.

Extracellular Matrix Alterations in Chronic Ischemic Cardiomyopathy Revealed by Quantitative Proteomics

This study uses quantitative proteomics to identify ECM protein alterations in end-stage ICM, revealing key upregulated components and pathways involved in adverse remodeling.

Deletion of Cd248 in Postn positive myofibroblast Fails to Attenuate Cardiac Remodeling and Fibrosis in a Murine Model of Pressure-Overload Cardiomyopathy

This study tests if deleting Cd248 in Postn+ myofibroblasts reduces cardiac fibrosis in pressure-overload cardiomyopathy, but finds no significant improvement in cardiac function or fibrosis.

INTERLEUKIN-18 AS A THERAPEUTIC TARGET FOR WESTERN DIET-INDUCED CARDIOMYOPATHY

This study shows that blocking IL-18 with IL-18BP improves cardiac function in mice on a Western diet, independent of weight gain and glucose tolerance.

Acute kidney injury disrupts cardiac remodeling via SerpinA3N

This study shows that acute kidney injury increases SerpinA3N in the heart, which inhibits serine protease activity and promotes cardiac fibrosis and remodeling.

Macrophage-derived CCL24 promotes fibrosis and worsens cardiac dysfunction during heart failure

This study shows that macrophage-derived CCL24 worsens fibrosis and cardiac dysfunction in heart failure by activating fibroblasts through the CCR3 receptor.

Embryonic Atrial Injury Programs an Anti-Fibrotic Atrial Fibrillation Substrate

This study shows that embryonic atrial injury leads to anti-fibrotic changes in adult atria through GPNMB-mediated mechanisms, preventing fibrosis.

Genetic inhibition of IL-12β suppresses systolic overload-induced cardiac inflammation and heart failure development

This study shows that genetic inhibition of IL-12β reduces cardiac inflammation and heart failure in mice subjected to transverse aortic constriction.

Single-cell transcriptomics and machine learning reveal RNF144B and C5AR1 as immune-related biomarkers and therapeutic targets in myocardial infarction

This paper identifies a 13-gene signature, including RNF144B and C5AR1, associated with myocardial infarction through transcriptomics and machine learning, highlighting their role in immune modulation and suggesting CCX168 as a therapeutic candidate.

Interferon gamma signaling drives cardiac metabolic rewiring

This study shows that IFN-gamma signaling in cardiomyocytes causes metabolic changes in the heart, including increased glucose uptake and reduced oxidative phosphorylation, which resemble changes in aging and heart failure.

NGAL drives cardiac dysfunction and fibrosis in rats with chronic kidney disease

This study shows that NGAL contributes to cardiac dysfunction and fibrosis in CKD rats through a Gal-3/Tlr4 pathway, with implications for human HFpEF.

Inhibition of Cardiac p38 Highlights the Role of the Phosphoproteome in Heart Failure Progression

This study investigates the effects of p38 MAPK inhibition on cardiac remodeling in a guinea pig HF model, finding that SB203580 treatment protects cardiac function and phosphoproteome integrity.

Multi-omic Profiling of Senescence Following Myocardial Infarction Reveals Dynamic Characteristics in Cardiac Remodeling

This study uses multi-omic profiling to show that senescent cells, particularly late myofibroblasts, transiently contribute to cardiac remodeling after myocardial infarction.

Targeting RUNX1 in Macrophages Facilitates Cardiac Recovery

This study identifies RUNX1 as a key regulator of cardiac recovery by reprogramming macrophages, showing that its inhibition promotes heart function recovery in a chronic heart failure model.

Isoliensinine Ameliorates Pathological Cardiac Hypertrophy After Aerobic Exercise by Activating Cytochrome c Oxidase Subunit 6A2

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.

Adiponectin-receptor agonism prevents right ventricular tissue pathology in a mouse model of Duchenne muscular dystrophy

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