Cardiac Fibrosis and Remodeling

This study shows that macrophage extracellular traps (METs) contribute to heart failure by promoting cardiac remodelling through PAD4-dependent mechanisms, and targeting METs may offer therapeutic potential.

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.

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.

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

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

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.

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

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.

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

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.

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

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.

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

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.

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

This study shows that deleting β2AR in myeloid cells improves cardiac function and reduces fibrosis after heart attack by enhancing efferocytosis of neutrophils.

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.

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.

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

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.

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

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.

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.

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.

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.

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

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.

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.