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Injury-Induced CLU-Positive Cardiomyocytes Drive Metabolic Reprogramming of Macrophage Function in Heart Regeneration

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE254058 | GEO | 2025/11/24

REPOSITORIES: GEO

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Injury-Induced CLU-Positive Cardiomyocytes Drive Metabolic Reprogramming of Macrophage Function in Heart Regeneration [10X_chromium]

Project description:The regenerative capacity of the adult mammalian heart is constrained by the post-mitotic nature of cardiomyocytes (CMs). Conversely, neonatal mouse hearts exhibit a regenerative window within the first week of life. Here, we demonstrate that an injury-induced Clusterin-positive (Clu+) CM population reprograms macrophages, facilitating heart regeneration during this timeframe. Clu+ CMs are selectively induced in the border zone of regenerative hearts across multiple species, contrasting with their absence in non-regenerative hearts. Genetic ablation of Clu+ CMs or Clu impedes neonatal heart regeneration, while transplantation of engineered human organoids enriched in Clu+ CMs or Clu overexpression promotes myocardial regeneration in adult mice. Mechanistically, Clu+ CMs secrete CLU, binding to TLR4 in macrophages, directing them toward an immune-suppressive neonatal-like phenotype through Cpt1a-mediated metabolic reprogramming, inducing BMP2 and promoting CM proliferation. Our findings unveil a novel cellular source for mammalian heart regeneration and highlight the fundamental roles of cardio-immune interaction in cardiac repair.

2025-11-24 | GSE253859 | GEO

Injury-Induced CLU-Positive Cardiomyocytes Drive Metabolic Reprogramming of Macrophage Function in Heart Regeneration [stero-seq]

2025-11-24 | GSE254056 | GEO

Injury-Induced CLU-Positive Cardiomyocytes Drive Metabolic Reprogramming of Macrophage Function in Heart Regeneration [Spatial Transcriptomics]

2025-11-24 | GSE254055 | GEO

Injury-Induced CLU-Positive Cardiomyocytes Drive Metabolic Reprogramming of Macrophage Function in Heart Regeneration

Project description:Injury-Induced CLU-Positive Cardiomyocytes Drive Metabolic Reprogramming of Macrophage Function in Heart Regeneration

| PRJNA1068444 | ENA

Injury-Induced CLU-Positive Cardiomyocytes Drive Metabolic Reprogramming of Macrophage Function in Heart Regeneration [10X_chromium]

Project description:Injury-Induced CLU-Positive Cardiomyocytes Drive Metabolic Reprogramming of Macrophage Function in Heart Regeneration [10X_chromium]

| PRJNA1067571 | ENA

Injury-Induced CLU-Positive Cardiomyocytes Drive Metabolic Reprogramming of Macrophage Function in Heart Regeneration [Spatial Transcriptomics]

Project description:Injury-Induced CLU-Positive Cardiomyocytes Drive Metabolic Reprogramming of Macrophage Function in Heart Regeneration [Spatial Transcriptomics]

| PRJNA1068456 | ENA

Injury-Induced CLU-Positive Cardiomyocytes Drive Metabolic Reprogramming of Macrophage Function in Heart Regeneration [stero-seq]

Project description:Injury-Induced CLU-Positive Cardiomyocytes Drive Metabolic Reprogramming of Macrophage Function in Heart Regeneration [stero-seq]

| PRJNA1068455 | ENA

Metabolic reprogramming and membrane glycans remodelling drive zebrafish heart regeneration

Project description:label-free relative quantitation based on nLC-MS/MS performed on heart tissues in a clinically relevant zebrafish model of cardiac tissue regeneration . Each of the six samples (2dp Cl, 2dpS, 7dp Cl, 7dpS, 14dp Cl, 14dpS,) has been analysed in two technical replicates. dpci = days post cryoinjury; dps = days post sham

2022-11-14 | MSV000090703 | MassIVE

GNPS - Metabolic reprogramming and membrane glycans remodelling drive zebrafish heart regeneration

2022-11-14 | MSV000090703 | GNPS

Macrophage LMO7 deficiency facilitates inflammatory injury <i>via</i> metabolic-epigenetic reprogramming.

Project description:Inflammatory bowel disease (IBD) is a formidable disease due to its complex pathogenesis. Macrophages, as a major immune cell population in IBD, are crucial for gut homeostasis. However, it is still unveiled how macrophages modulate IBD. Here, we found that LIM domain only 7 (LMO7) was downregulated in pro-inflammatory macrophages, and that LMO7 directly degraded 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3) through K48-mediated ubiquitination in macrophages. As an enzyme that regulates glycolysis, PFKFB3 degradation led to the glycolytic process inhibition in macrophages, which in turn inhibited macrophage activation and ultimately attenuated murine colitis. Moreover, we demonstrated that PFKFB3 was required for histone demethylase Jumonji domain-containing protein 3 (JMJD3) expression, thereby inhibiting the protein level of trimethylation of histone H3 on lysine 27 (H3K27me3). Overall, our results indicated the LMO7/PFKFB3/JMJD3 axis is essential for modulating macrophage function and IBD pathogenesis. Targeting LMO7 or macrophage metabolism could potentially be an effective strategy for treating inflammatory diseases.

| S-EPMC10692378 | biostudies-literature

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