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GSDME-controlled pyroptosis promotes muscle repair by coordinating tissue resident macrophages and fibro-adipogenic progenitors

ABSTRACT: GSDME (Gasdermin E) is a critical protein known for its role in pyroptosis, a form of programmed cell death associated with inflammation. We demonstrated that GSDME as a crucial mediator in muscle repair, particularly in the context of muscle damage induced by cardiotoxin (CTX). Specifically, we found that GSDME-controlled pyroptosis promotes muscle repair by coordinating the activities of tissue-resident macrophages and fibro-adipogenic progenitors (FAPs).

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse-phase, Liquid Chromatography MS - positive - reverse-phase

PROVIDER: MTBLS10509 | MetaboLights | 2026-01-05

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS10509_LC-MS_negative_reverse-phase_metabolite_profiling.txt	Txt
	a_MTBLS10509_LC-MS_positive_reverse-phase_metabolite_profiling.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS10509_LC-MS_negative_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular
	m_MTBLS10509_LC-MS_positive_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular

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Similar Datasets

GSDME-controlled pyroptosis promotes muscle repair by coordinating tissue resident macrophages and fibro-adipogenic progenitors

Project description:GSDME (Gasdermin E) is a critical protein known for its role in pyroptosis, a form of programmed cell death associated with inflammation. We demonstrated that GSDME as a crucial mediator in muscle repair, particularly in the context of muscle damage induced by cardiotoxin (CTX). Specifically, we found that GSDME-controlled pyroptosis promotes muscle repair by coordinating the activities of tissue-resident macrophages and fibro-adipogenic progenitors (FAPs).

2025-12-12 | GSE270614 | GEO

GSDME-controlled pyroptosis promotes muscle repair by coordinating tissue resident macrophages and fibro-adipogenic progenitors [RNA-seq]

2025-12-12 | GSE271087 | GEO

GSDME-controlled pyroptosis promotes muscle repair by coordinating tissue resident macrophages and fibro-adipogenic progenitors

Project description:GSDME-controlled pyroptosis promotes muscle repair by coordinating tissue resident macrophages and fibro-adipogenic progenitors

| PRJNA1127567 | ENA

GSDME-controlled pyroptosis promotes muscle repair by coordinating tissue resident macrophages and fibro-adipogenic progenitors [RNA-seq]

Project description:GSDME-controlled pyroptosis promotes muscle repair by coordinating tissue resident macrophages and fibro-adipogenic progenitors [RNA-seq]

| PRJNA1129589 | ENA

Nigericin induced paraptosis-like cell death instead of pyroptosis in corneal keratocytes

Project description:Corneal wound healing involves complex cellular processes, including keratocyte cell death, which plays a pivotal role in initiating tissue repair. Recent studies suggest that pyroptosis, characterized by the release of pro-inflammatory factors, occurs during tissue repair which may also contribute to the inflammatory phase of corneal wound healing. In this study, we investigated the nature of cell death in human keratocytes treated with nigericin, a known pyroptosis inducer. Surprisingly, nigericin triggered a unique form of non-inflammatory cell death marked by extensive vacuolation, resembling paraptosis. Proteomic analysis revealed that our human keratocytes lack key components of the canonical pyroptosis pathway, including NLRP3, ASC, and caspase-1, potentially explaining the absence of pyroptosis in these cells. This process was further confirmed by the absence of caspase-3 activation and lack of ER stress, alongside increased autophagic marker LC3-II accumulation. These findings suggest that nigericin triggers a paraptosis-like cell death in keratocytes, rather than pyroptosis, highlighting an alternative mechanism of cell death in corneal wound healing that warrants further exploration.

2025-06-30 | PXD058468 | Pride

Dimethyl Itaconate alleviates the pyroptosis of macrophages through oxidative stress

Project description:Macrophages are involved in the pathophysiology of many diseases as critical cells of the innate immune system. Pyroptosis is a form of macrophage death that induces cytokinesis of phagocytic substances in the macrophages, thereby defending against infection. Dimethyl itaconate (DI) is an analog of itaconic acid with anti-inflammatory effects. However, the effect of dimethyl itaconate on macrophage pyroptosis has not been elucidated clearly. Thus, the present study aimed to analyze the effect of DI treatment on a macrophage pyroptosis model (Lipopolysaccharide, LPS+Adenosine Triphosphate, ATP). The results showed that 0.25 mM DI ameliorated macrophage pyroptosis and downregulated interleukin (IL)-1β expression. Then, real-time quantitative polymerase chain reaction (RT-qPCR) was used to confirm the result of RNA-sequencing of the upregulated oxidative stress-related genes (Gclc and Gss) and downregulated inflammation-related genes (IL-12β and IL-1β). In addition, Gene Ontology (GO) enrichment analysis showed that differential genes were associated with transcript levels and DNA replication. Kyoto encyclopedia of genes and genomes (KEGG) enrichment showed that signaling pathways, such as tumor necrosis factor (TNF), Jak, Toll-like receptor and IL-17, were altered after DI treatment. N-acetyl-L-cysteine (NAC) reversed the DI effect on the LPS+ATP-induced macrophage pyroptosis and upregulated the IL-1β expression. Oxidative stress-related protein Nrf2 is involved in the DI regulation of macrophage pyroptosis. Taken together, these findings suggested that DI alleviates the pyroptosis of macrophages through oxidative stress.

2021-10-16 | GSE185895 | GEO

ROS-Responsive Potassium Ionophore-Based Nanoplatform Potentiates Cancer Pyroptosis-Immunotherapy via ER Stress

Project description:Pyroptosis is an emerging programmed cell death with great potential in antitumor immunotherapy. However, the actual application of pyroptosis is hampered by its nonspecificity and inefficiency. In this study, a reactive oxygen species (ROS) responsive potassium (K+) ionophore-based nanoplatform rPPAA18C6 is constructed based on the triblock polymers PEG-PPBAEM-PAA18C6 to potentiate cancer pyroptosis and immunotherapy via the K+ metabolic disturbance mediated endoplasmic reticulum (ER) stress. The PEG (P) is used to prolong the circulation time in vivo, PPBAEM (r) is used to target the tumor cells and responds to the higher ROS, and PAA18C6 is used to perturb of K+ homeostasis. Moreover, rPPAA18C6 can also function as a drug carrier for chemodrug (doxorubicin, Dox). We find that rPPAA18C6@Dox provokes immune responses in melanoma (B16F10) via pyroptosis-related immunogenic cell death (ICD), in which damage-associated molecular patterns (DAMPs) are released to promote maturation of dendritic cells (DCs), activate cytotoxic T lymphocytes (CTLs), and convert immunosuppressive “cold” tumor to immunogenic “hot” tumor. Moreover, the combined therapy with anti-PD-L1 exhibits apparent tumor suppression far more than expected, suggesting a powerful candidate of rPPAA18C6@Dox for high-efficient immune checkpoint blockade (ICB) therapy. This study thus provides a promising strategy to specifically initiate pyroptosis and potentiate immunotherapy by perturbation of K+ metabolism via a smart nanoplatform.

2025-01-01 | GSE256169 | GEO

Targeting pyroptosis with nanoparticles to alleviate neuroinflammatory for preventing secondary damage following traumatic brain injury

Project description:Post-traumatic neuroinflammation is a key driver of secondary injury after traumatic brain injury (TBI). Pyroptosis, a proinflammatory form of programmed cell death, considerably activates strong neuroinflammation and amplifies the inflammatory response by releasing inflammatory contents. Therefore, treatments targeting pyroptosis may beneficially effects for the treatment of secondary brain damage after TBI. Herein, a cysteine-alanine-glutamine-lysine (CAQK) peptide-modified β-lactoglobulin (β-LG) nanoparticle was constructed to deliver disulfiram (DSF), C-β-LG/DSF, to inhibit pyroptosis and decrease neuroinflammation, thereby preventing TBI-induced secondary injury. In the post-TBI mice model, C-β-LG/DSF selectively targets the injured brain, increases DSF accumulation, and extends the time of the systemic circulation of DSF. C-β-LG/DSF can alleviate brain edema and inflammatory response, inhibit secondary brain injury, promote learning, and improve memory recovery in mice after trauma. Therefore, this study likely provided a new approach for reducing the secondary spread of TBI.

2024-01-17 | GSE244966 | GEO

Innate immune sensing of influenza virus through IFI16 promote pyroptosis.

Project description:We report that IFI16, which was previously identified as a cytosolic DNA sensor, is essential for the activation of programmed cell death pathways in IAV infected cells. We have identified IFI16 as an innate immune sensor of the influenza A virus. We find that IFI16 recognizes viral genomic RNA upon infection. The activation of IFI16, in turn, triggers the production of type I, III interferons, and also other pro-inflammatory cytokines via the STING-TBK1 and Pro-caspase-1 signalling axis, thereby promoting cell death (apoptosis and pyroptosis in IAV infected cells).

2021-12-31 | GSE163705 | GEO

Nur77 induces GSDMC-mediated pyroptosis

Project description:Pyroptosis is a type of lytic cell death executed by members of the gasdermin family. It has been demonstrated that induction of pyroptosis can effectively inhibit tumor growth, which implicates a new strategy for clinical tumor therapy, especially for those tumors (such as melanoma) that are insensitive or resistant to the induction of apoptosis.By means of a chemical compound DBIC, designed and identified by our group recently, to induce GSDMC-mediated pyroptosis in melanoma cells.

2025-07-07 | GSE273365 | GEO

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