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Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics

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

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE242821 | GEO | 2025/04/03

REPOSITORIES: GEO

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Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [Spatial Transcriptomics]

Project description:Oxidative phosphorylation defects results in mitochondrial diseases, with cardiac involvement markedly impacting prognosis. However, the mechanisms underlying the transition from compensation to dysfunction in response to metabolic deficiency remain unclear, impeding the development of effective treatments. Here, we employed single-nucleus RNA sequencing (snRNA-seq) on hearts from mitochondrial cardiomyopathy (MCM) mice with cardiac-specific Ndufs6 knockdown of (FS6KD). Pseudotime trajectory analysis of cardiomyocytes from early stage of female FS6KD hearts revealed dynamic cellular state transitioning from compensation to severe compromise, coincided with transient upregulation of a critical transcription factor, activating transcription factor 3 (Atf3). Genetic ablation or adeno-associated virus-mediated Atf3 knockdown in FS6KD mice effectively delayed cardiomyopathy progression in a female-specific manner. Notably, human MCM snRNA-seq revealed a similar transition, including the dynamic expression of ATF3. In conclusion, our findings highlight a fate-determining role of Atf3 in female MCM progression, providing a promising therapeutic candidate for the currently intractable disease.

2025-04-03 | GSE282635 | GEO

Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [RNA-seq]

2025-04-03 | GSE242819 | GEO

Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [PIC_RNA-seq]

2025-04-03 | GSE242818 | GEO

Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [snRNA-seq]

2025-04-03 | GSE242820 | GEO

Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics

Project description:Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics

| PRJNA1014902 | ENA

Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [Spatial Transcriptomics]

Project description:Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [Spatial Transcriptomics]

| PRJNA1189511 | ENA

Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [RNA-seq]

Project description:Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [RNA-seq]

| PRJNA1014956 | ENA

Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [snRNA-seq]

Project description:Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [snRNA-seq]

| PRJNA1014957 | ENA

Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [PIC_RNA-seq]

Project description:Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by single-cell transcriptomics [PIC_RNA-seq]

| PRJNA1014897 | ENA

Single-cell and spatial transcriptomics reveal a potential role of ATF3 in brain metastasis of lung adenocarcinoma.

Project description:BackgroundBrain metastasis (BrM) has been a challenge for lung cancer treatment, but the mechanisms underlying lung cancer BrM remain elusive. This study aims to dissect cellular components and their spatial distribution in human BrM tumors of lung adenocarcinoma (LUAD) and identify potential therapeutic targets.MethodsWe performed single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST) on three LUAD BrMs, and validated our findings using public scRNA-seq data of 10 LUAD BrMs. Western blotting, quantitative real-time polymerase chain reaction (qRT-PCR) and functional experiments were employed for experimental studies.ResultsBy combining scRNA-seq and ST, our analysis revealed the inter- and intra-tumoral heterogeneity of cellular components and their spatial localization within LUAD BrMs. Through RNA velocity and transcription factor (TF) regulatory activity analyses, we identified ATF3 as a potential regulator of the mesenchymal-epithelial transition (MET) program, which plays crucial roles in the colonization of tumor cells at metastatic sites. Furthermore, we demonstrated that knockdown of ATF3 significantly inhibited cancer cell proliferation while promoting cancer cell migration. Mechanistically, ATF3 knockdown could reverse the MET program. Additionally, we revealed that LGALS3/ANXA2-mediated cell-cell interaction between macrophage and tumor cells may also promote the MET program.ConclusionsOur study provides a single-cell atlas of the cellular composition in BrM of LUAD and identifies ATF3 as a potential therapeutic target for BrM treatment.

| S-EPMC11826269 | biostudies-literature

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