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

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).

ORGANISM(S): Mus musculus

PROVIDER: GSE271087 | GEO | 2025/12/12

REPOSITORIES: GEO

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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

Revealing disulfide bond formation in GSDME upon UVC irradiation under non-reducing conditions

Project description:It is widely acknowledged that gasdermin family proteins, which are known as the executors of pyroptosis, undergo protease-mediated cleavage prior to inducing pyroptosis. Here, we unexpectedly discovered a non-canonical form of pyroptosis mediated by full-length GSDME (FL-GSDME) without any proteolytic cleavage. Upon intense ultraviolet (UV) irradiation-triggered DNA damage, hyperactivation of nuclear PARP1 led to extensive formation of poly(ADP-ribose) (PAR) polymers and then release to the cytoplasm.These PAR polymers activate PARP5 to catalyze GSDME PARylation, resulted in a conformational change in GSDME that relieved autoinhibition imposed by its C terminus on the N terminus. On the other hand, intense UV irradiation boosted mitochondrial fission-dependent generation of mitochondrial reactive oxygen species (mito-ROS), further promoting cytochrome c-catalyzed peroxidation of cardiolipin. This lipid-ROS signal was then sensed by PARylated-GSDME and then induced oxidative oligomerization of GSDME, which facilitated FL-GSDME plasma membrane targeting for perforation, eventually inducing pyroptosis. Reagents that concurrently stimulate PARPs activity and lipid-ROS also induced sequential modifications i.e., PARylation and oxidation of FL-GSDME and synergistically promoted pyroptotic cell death. Overall, our findings elucidate a novel mechanism underlying cleavage-independent function of GSDME in executing cell demise, further enriching the paradigms and cognition of FL-GSDME-mediated non-canonical pyroptosis.

2024-06-17 | PXD051840 | Pride

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

The collaboration of GSDMD and GSDME in folic acid (FA)-induced renal injury

Project description:Acute kidney injury(AKI) is associated with an increased risk of chronic kidney disease(CKD). There is still a lack of effective prevention for AKI-CKD transition. In the present study, we simultaneously explored the contribution of GSDMD and GSDME in folic acid (FA)-induced nephropathy, a model mimicking the essential components of the AKI-CKD transition. We found that blockage of both GSDMD and GSDME-mediated pyroptosis could have accumulative protection against FA-induced AKI-CKD transition. GSDME-mediated pyroptosis played a crucial role in tubular cell damage. GSDMD could exert important functions in infiltration of inflammatory cells and NETs formation. Pyroptotic tubular cells triggered NETs generation and macrophage polarization. NETs promoted macrophage-to-myofibroblast transition. Our results illustrated the orchestration of GSDMD and GSDME in AKI-CKD transition, providing new insights into the molecular mechanism for the clinical dilemma.

2024-10-31 | GSE245446 | GEO

Anti-PD-1 exacerbates bleomycin-induced lung injury in mice via Caspase-3/GSDME-mediated pyroptosis

Project description:To revealed the significant involvement of GSDME-mediated pyroptosis in the pathogenesis and development of ICI-LI

2024-12-23 | GSE280068 | GEO

Pyroptosis modulates multiple immune cell populations in targeted therapy-treated melanoma

Project description:Treatment of melanoma with BRAF inhibitors plus MEK inhibitors (BRAFi + MEKi) stimulates an intratumoral immune response, in part through pyroptosis mediated by the pore-forming protein gasdermin E (GSDME/Gsdme). How GSDME-mediates effects on tumoral immunity is not well characterized. Using single-cell RNA-sequencing (scRNA-seq) and flow cytometry, we show that Gsdme knockout (KO) tumors have decreased infiltration of T cells, natural killer (NK) cells and regulatory T cells (Tregs) following BRAFi + MEKi-treatment compared to control tumors. Infiltrated Tregs in Gsdme KO tumors displayed decreased expression of the interleukin 2 receptor and phenotypic markers that are associated with a suppressive function of Tregs. Furthermore, intratumoral, phenotypically suppressive Tregs were decreased after BRAFi + MEKi treatment in Gsdme KO tumors expressing a pyroptosis-defective mutant form of Gsdme (T6E) compared to tumors expressing wild-type Gsdme. Use of a TLR9 agonist, which alters the tumor immune microenvironment, decreased the regrowth of Gsdme KO tumors on BRAFi + MEKi treatment, correlating to a further decrease in intratumoral Tregs. Overall, we show a critical role of GSDME in the modulation of intratumoral immune cells, particularly Tregs, in BRAFi + MEKi-treated melanoma.

2025-11-20 | GSE308595 | GEO

Gasdermin E is Dispensable for H1N1 Influenza Virus Pathogenesis in Mice

Project description:Targeting cell death pathways, including pyroptosis and necroptosis, has been shown to mitigate influenza virus infection severity. Here, we examined whether pyroptosis specifically driven by the pore-forming protein gasdermin E (GSDME) is involved in regulating influenza virus infection outcomes. We found that Gsdme-/- mice showed similar weight loss and survival in severe A/PR/8/34 (H1N1) virus infections compared to WT counterparts. Likewise, lung dysfunction, histopathological damage, viral titers, and inflammatory cytokine levels were similar in the two groups. Global transcriptomic analysis also revealed similar gene expression programs in WT versus Gsdme-/- mouse lungs at baseline and in response to infection. To confirm the generality of these findings, we infected mice with 2009 pandemic H1N1 virus and again observed similar weight loss, mortality, and lung dysfunction in WT and Gsdme-/- mice. Our results overall demonstrate that GSDME contributes negligibly to the host response against H1N1 influenza virus, refining our understanding of cell death pathways in influenza pathogenesis.

2025-11-19 | GSE302673 | GEO

A novel non-nad-based PARP1 inhibitor, Japoflavone B, triggered Caspase-3/GSDME-mediated pyroptosis through ROS/p38/p53 pathway in NSCLC

Project description:It’s an effective anti-cancer strategy to study natual products for activating GSDME-mediated pyroptosis through targeting PARP-1 in NSCLC. Previously, we found that a novel flavonoid Japoflavone B (JFB) has exhibited an excellent inhibitory activity against cancer cell proliferation in vitro study, but its in vivo and mechanism study are still unknown. Herein, JFB could specifically inhibit the proliferation of NSCLC cells, but not normal lung epithelial cells. JFB induced inflammatory pyroptosis through the activation of caspase-3 and GSDME cleavage. JFB also activated caspase-3/7/9 activities and triggered mitochondria-mediated apoptosis. Its inhibitory activity would be significantly reversed with the caspase-3 or GSDME deficiencies and their specific inhibitors. JFB could targetedly inhibit PARP-1 activity, and promote DNA damage and ROS accumulation. Meanwhile, JFB could significantly promote p-p38 and p53 expression. Then, JFB induced cell cycle G2/M arrest by reprogramming the expression of cyclins, CDKs and CKIs. Moreover, its cytotoxicity could be dramatically reversed with the ROS scavenger and p38 inhibitor. In vivo, JFB exhibited a comparable anti-tumor activity to that of Dox with no significant tissue toxicity. Our data firstly revealed that JFB functions as a selective and non-NAD-based PARP inhibitor with high affinity and low toxicology, which makes it potential to develop as a lead anti-cancer compound. As well, JFB promoted caspase-3/GSDME-mediated pyroptosis through ROS/p38/p53 pathway in NSCLC cells. Our study was further enriched the specific mechanism that PARP inhibitor could trigger caspase-3/GSDME-mediated pyroptosis through ROS/p38/p53 pathway in NSCLC cells.

2025-11-09 | GSE281636 | GEO

Myeloid cell analysis during a pro-fibrotic ischemia-reperfusion and cardiotoxin muscle injury.

Project description:Myeloid cells are critical to the development of fibrosis following muscle injury, however, the mechanism of their role in fibrosis formation remains unclear. Here we demonstrate that myeloid cell-derived TGF-β1 signaling is increased in a pro-fibrotic ischemia-reperfusion and cardiotoxin (IR/CTX) muscle injury model. This study analyzes scRNAsequencing from the fibrotic region after a pro-fibrotic ischemia-reperfusion and cardiotoxin muscle injury.

2020-01-28 | GSE144270 | GEO

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