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STING aggravates ferroptosis-dependent myocardial ischemia-reperfusion injury by targeting GPX4 for autophagic degradation

ABSTRACT: STING aggravates ferroptosis-dependent myocardial ischemia-reperfusion injury by targeting GPX4 for autophagic degradation

PROVIDER: PRJNA1233788 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32624602_1.fastq.gz	Fastqsanger.gz
	SRR32624602_2.fastq.gz	Fastqsanger.gz
	SRR32624603_1.fastq.gz	Fastqsanger.gz
	SRR32624603_2.fastq.gz	Fastqsanger.gz
	SRR32624604_1.fastq.gz	Fastqsanger.gz

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STING aggravates ferroptosis-dependent myocardial ischemia-reperfusion injury by targeting GPX4 for autophagic degradation

Project description:To investigate the potential signal pathways affected by the deletion of the Sting gene in mice during ischemia-reperfusion (IR), we extracted the myocardial tissues of mice 24 hours after ischemia-reperfusion. Subsequently, we conducted gene expression profiling analysis using the data obtained from RNA-seq of STING-CKO mice and their control counterparts.

2025-04-10 | GSE291453 | GEO

miR-135b-3p Promotes Cardiomyocyte Ferroptosis by Targeting GPX4 and Aggravates Myocardial Ischemia/Reperfusion Injury.

Project description:Ferroptosis is a form of cell death induced by excess iron and accumulation of reactive oxygen species in cells. Recently, ferroptosis has been reported to be associated with cancer and ischemia/reperfusion (I/R) injury in multiple organs. However, the regulatory effects and underlying mechanisms of myocardial I/R injury are not well-understood. The role of miR-135b-3p as an oncogene that accelerates tumor development has been confirmed; however, its role in myocardial I/R is not fully understood. In this study, we established an in vivo myocardial I/R rat model and an in vitro hypoxia/reoxygenation (H/R)-induced H9C2 cardiomyocyte injury model and observed that ferroptosis occurred in tissues and cells during I/R myocardial injury. We used database analysis to find miR-135b-3p and validated its inhibitory effect on the ferroptosis-related gene glutathione peroxidase 4 (Gpx4), using a luciferase reporter assay. Furthermore, miR-135b-3p was found to promote the myocardial I/R injury by downregulating GPX4 expression. The results of this study elucidate a novel function of miR-135b-3p in exacerbating cardiomyocyte ferroptosis, providing a new therapeutic target for improving I/R injury.

| S-EPMC8414249 | biostudies-literature

Knockout of GPx4 gene in mouse keratinocyte

Project description:Comparative analysis of gene expression in cultured primary keratinocytes isolated from newborn control (K14-cre; GPx4fl/+) and knockout (K14-cre; GPx4fl/fl) mice. Selenoproteins are essential for skin function, as targeted abolition of selenoproteins in epidermal tissue results in newborn mice manifesting gross abnormalities of skin and hair, accompanied by retarded growth and premature death. To investigate whether lack of a single selenoprotein could induce similar phenotypic effect in mice, we generated keratinocyte-specific knockout mice lacking glutathione peroxidase 4 (GPx4), an essential selenoprotein in skin, to examine phenotypic changes resulting from the lack of GPx4 in skin. Ablation of GPx4 results in focal alopecia and disturbed hair follicle morphogenesis, with GPx4 being essential during early stages of hair follicle morphogenesis as well as for keratinocyte adhesion and proliferation in culture. We have generated mice with selective removal of the GPx4 gene in keratinocytes under the control of Keratin-14-cre (K14-cre) promoter. Comparative microarray analysis was performed on RNA samples taken from pooled primary keratinocytes from knockout and control mice from the same litter. Array replicates were performed using RNA samples from three different litters.

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SESN1 alleviates autoimmunity by potentiating STING autophagic degradation

Project description:STING, the pivotal adaptor protein of CGAS-STING signaling, is critical for type I IFN production of innate immunity. However, excessive or prolonged activation of STING is associated with autoinflammatory and autoimmune diseases. Thus, preventing STING from over-activation is important to maintain immune homeostasis. Here, we reported that SESN1 was essential to prevent the excessive activation of STING-mediated type I IFN signaling through autophagic degradation of STING.

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Autophagy of OTUD5 Destabilizes GPX4 to Confer Ferroptosis-Dependent Kidney Injury

Project description:Ferroptosis is an iron-dependent programmed cell death associated with severe kidney diseases, linked to decreased glutathione peroxidase 4 (GPX4). However, the spatial distribution of renal GPX4-mediated ferroptosis and the molecular events causing GPX4 reduction during ischemia-reperfusion (I/R) remain largely unknown. Using spatial transcriptomics, we identify that GPX4 is situated at the interface of the inner cortex and outer medulla, a hyperactive ferroptosis site post-I/R injury. We show that OTU deubiquitinase 5 (OTUD5) is a GPX4-binding protein that confers ferroptosis resistance by stabilizing GPX4. During I/R, ferroptosis is induced by mTORC1-mediated autophagy, causing OTUD5 degradation and subsequent GPX4 decay. Functionally, OTUD5 deletion intensifies renal tubular cell ferroptosis and exacerbates acute kidney injury, while AAV-mediated OTUD5 delivery mitigates ferroptosis and promotes renal function recovery from I/R injury. In this work, our study highlights a new autophagy-dependent ferroptosis module: hypoxia/ischemia-induced OTUD5 autophagy triggers GPX4 degradation, offering a potential therapeutic avenue for I/R-related kidney diseases.

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METTL3 deficiency aggravates hepatic ischemia/reperfusion injury in mice by activating the MAPK signaling pathway

Project description:Inflammatory responses, apoptosis, and oxidative stress, are key factors that contribute to hepatic ischemia/reperfusion (I/R) injury, which may lead to the failure of liver surgeries, such as hepatectomy and liver transplantation. The N6-methyladenosine (m6A) modification has been implicated in multiple biological processes, and its specific role and mechanism in hepatic I/R injury require further investigation. We found that METTL3 may be involved in regulating this process. Therefore, we constructed an ischemia-reperfusion model with Hepatocyte-specific METTL3 knockdown (HKD) mice, and performed RNA- sequencing analysis with wild-type mice as controls.

2024-04-22 | GSE252255 | GEO

METTL3 deficiency aggravates hepatic ischemia/reperfusion injury in mice by activating the MAPK signaling pathway

Project description:METTL3 deficiency aggravates hepatic ischemia/reperfusion injury in mice by activating the MAPK signaling pathway

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Single-cell RNA Sequencing of Pig Lung Transplantation Reveals Macrophage Ferroptosis in Lung Ischemia‒Reperfusion Injury

Project description:Primary graft dysfunction (PGD), which is caused primarily by ischemia–reperfusion injury (IRI), is a major obstacle in lung transplantation. Here, we developed an orthotopic, single-lung transplant pig model to simulate prolonged cold IRI. After 24 hours of cold ischemia and 8 hours of warm reperfusion, the transplanted lung exhibited severe allograft injury. Subsequent single-cell RNA sequencing (scRNA-seq) revealed significant changes in alveolar macrophages after IRI, with prominently enriched ferroptosis pathways. Transmission electron microscopy (TEM) confirmed characteristic ferroptosis changes in lung macrophages, and decreased GPX4 expression in macrophages indicated increased susceptibility to ferroptosis. Overall, our pig orthotopic left lung transplant model effectively simulates IRI after transplantation, which offers a valuable platform for more detailed investigations of early reperfusion injury to pulmonary grafts. Moreover, we preliminarily demonstrated the importance of macrophage ferroptosis in IRI, suggesting that inhibiting macrophage ferroptosis may be a promising therapeutic strategy for lung IRI.

2025-04-22 | GSE293954 | GEO

SESN1 alleviates autoimmunity by potentiating STING autophagic degradation

Project description:SESN1 alleviates autoimmunity by potentiating STING autophagic degradation

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Inhibiting ATP6V0D2 Aggravates Liver Ischemia-Reperfusion Injury by Promoting NLRP3 Activation via Impairing Autophagic Flux Independent of Notch1/Hes1.

Project description:At present, liver ischemia-reperfusion (IR) injury is still a great challenge for clinical liver partial resection and liver transplantation. The innate immunity regulated by liver macrophages orchestrates the cascade of IR inflammation and acts as a bridge. As a specific macrophage subunit of vacuolar ATPase, ATP6V0D2 (V-ATPase D2 subunit) has been shown to promote the formation of autophagolysosome in vitro. Our research fills a gap which has existed in the study of inflammatory stress about the V-ATPase subunit ATP6V0D2 in liver macrophages. We first found that the expression of specific ATP6V0D2 in liver macrophages was upregulated with the induction of inflammatory cascade after liver IR surgery, and knockdown of ATP6V0D2 resulted in increased secretion of proinflammatory factors and chemokines, which enhanced activation of NLRP3 and aggravation of liver injury. Further studies found that the exacerbated activation of NLRP3 was related to the autophagic flux regulated by ATP6V0D2. Knocking down ATP6V0D2 impaired the formation of autophagolysosome and aggravated liver IR injury through nonspecific V-ATPase activation independent of V-ATPase-Notchl-Hesl signal axis. In general, we illustrated that the expression of ATP6V0D2 in liver macrophages was upregulated after liver IR, and by gradually promoting the formation of autophagolysosomes to increase autophagy flux to limit the activation of liver inflammation, this regulation is independent of the Notch1-Hes1 signal axis.

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