0
Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Human Health Effects Remediation Sign in to save

Gasdermins in sepsis

Frontiers in Immunology 2023 5 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 45 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Wenhua Wang, Zhihui He

Summary

This review covered the roles of gasdermin proteins in sepsis, examining how these pore-forming executors drive inflammatory cell death and cytokine release during the dynamic inflammatory and immune responses across different stages of the disease.

Body Systems

Sepsis is a hyper-heterogeneous syndrome in which the systemic inflammatory response persists throughout the course of the disease and the inflammatory and immune responses are dynamically altered at different pathogenic stages. Gasdermins (GSDMs) proteins are pore-forming executors in the membrane, subsequently mediating the release of pro-inflammatory mediators and inflammatory cell death. With the increasing research on GSDMs proteins and sepsis, it is believed that GSDMs protein are one of the most promising therapeutic targets in sepsis in the future. A more comprehensive and in-depth understanding of the functions of GSDMs proteins in sepsis is important to alleviate the multi-organ dysfunction and reduce sepsis-induced mortality. In this review, we focus on the function of GSDMs proteins, the molecular mechanism of GSDMs involved in sepsis, and the regulatory mechanism of GSDMs-mediated signaling pathways, aiming to provide novel ideas and therapeutic strategies for the diagnosis and treatment of sepsis.

Sign in to start a discussion.

More Papers Like This

Article Tier 2

Mechanism of Pyroptosis in Acute Liver Injury and Prospect of Targeted Therapy

This review examined the role of pyroptosis—an inflammatory form of programmed cell death—in acute liver injury, covering the gasdermin-mediated molecular mechanisms involved. The authors proposed that targeting pyroptosis pathways may offer new therapeutic strategies for conditions such as drug-induced liver injury and ischemia-reperfusion damage.

Article Tier 2

Gasdermin D-dependent macrophage pyroptosis mediates polystyrene microplastics-induced pulmonary fibrosis

Researchers demonstrated that chronic intranasal exposure to polystyrene microplastics in mice triggered a specific form of inflammatory cell death called pyroptosis in lung macrophages, leading to pulmonary fibrosis. The study identified the Gasdermin D protein as a key mediator of this process, suggesting a potential mechanistic pathway through which microplastic inhalation could contribute to lung tissue scarring.

Article Tier 2

The Anti-Oxidative, Anti-Inflammatory, Anti-Apoptotic, and Anti-Necroptotic Role of Zinc in COVID-19 and Sepsis

This review summarizes zinc's multiple protective roles in the body, including its anti-oxidative, anti-inflammatory, and cell-death-regulating properties, with a focus on relevance to severe infections like sepsis. Researchers describe how zinc modulates key immune pathways and inhibits specific enzymes involved in programmed cell death. The study highlights zinc's potential as a supportive nutritional element in managing inflammatory conditions.

Article Tier 2

Nanomaterial-induced pyroptosis: a cell type-specific perspective

This review examined how various nanomaterials induce pyroptosis (inflammatory cell death) across different non-tumorous cell types, analyzing the diverse pathways and mechanisms involved. The review highlights significant knowledge gaps regarding less-studied pyroptosis pathways and calls for more systematic investigation of nanomaterial-cell interactions.

Article Tier 2

Gasdermin D Deficiency Does Not Protect Mice from High-Fat Diet-Induced Glucose Intolerance and Adipose Tissue Inflammation

Researchers tested whether gasdermin D (GSDMD), a mediator of pyroptotic cell death, plays a role in obesity-related metabolic disease by studying GSDMD-deficient mice on a high-fat diet. GSDMD deficiency did not protect mice from glucose intolerance or adipose tissue inflammation, suggesting GSDMD is not a primary driver of obesity-associated metabolic dysfunction.

Share this paper