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Related Concept Videos

Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...

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Related Experiment Video

Updated: Jun 14, 2026

Cecal Ligation Puncture Procedure
11:53

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Published on: May 7, 2011

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Gasdermins in sepsis.

Wenhua Wang1, Zhihui He1,2

  • 1Department of Intensive Care Unit, the Third Xiangya Hospital, Central South University, Changsha, Hunan, China.

Frontiers in Immunology
|November 29, 2023
PubMed
Summary
This summary is machine-generated.

Gasdermins (GSDMs) proteins are key players in sepsis, mediating inflammatory cell death. Understanding GSDM functions offers promising therapeutic strategies to combat this complex syndrome and reduce mortality.

Keywords:
cell deathgasderminregulationsepsistherapy

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Area of Science:

  • Immunology
  • Molecular Biology
  • Pathophysiology

Background:

  • Sepsis is a complex, hyper-heterogeneous syndrome characterized by a persistent systemic inflammatory response.
  • Inflammatory and immune responses dynamically change throughout sepsis pathogenesis.
  • Gasdermins (GSDMs) are pore-forming proteins crucial for releasing inflammatory mediators and inducing inflammatory cell death.

Purpose of the Study:

  • To review the diverse functions of GSDMs proteins in the context of sepsis.
  • To elucidate the molecular mechanisms by which GSDMs contribute to sepsis.
  • To explore regulatory pathways of GSDMs-mediated signaling for novel therapeutic insights.

Main Methods:

  • Literature review focusing on GSDMs and sepsis.
  • Analysis of molecular mechanisms of GSDMs in inflammatory processes.
  • Examination of signaling pathways regulated by GSDMs.

Main Results:

  • GSDMs are central executors of inflammatory cell death in sepsis.
  • GSDMs mediate the release of pro-inflammatory cytokines, exacerbating the systemic response.
  • Dysregulation of GSDMs contributes to multi-organ dysfunction in sepsis.

Conclusions:

  • GSDMs represent a promising therapeutic target for sepsis treatment.
  • A deeper understanding of GSDMs' role can lead to improved diagnostic and therapeutic strategies.
  • Targeting GSDMs may alleviate multi-organ dysfunction and reduce sepsis-induced mortality.