Related Experiment Video
Updated: May 20, 2025

06:12
Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum
Published on: May 3, 2024
1.6K
Mechanistic insights into gasdermin-mediated pyroptosis
Yang Bai1, Youdong Pan2, Xing Liu3,4
1Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, China.
Nature Reviews. Molecular Cell Biology
|March 25, 2025
Summary
Pyroptosis is an inflammatory cell death process involving gasdermin (GSDM) proteins. Understanding GSDM-mediated pyroptosis offers potential for new treatments for inflammatory and autoimmune diseases.
Area of Science:
- Cell Biology
- Immunology
- Molecular Biology
Background:
- Pyroptosis is a programmed inflammatory cell death pathway.
- It is executed by gasdermin (GSDM) proteins.
- Pyroptosis plays roles in immunity, host defense, and disease pathogenesis.
Purpose of the Study:
- To review current knowledge on GSDM-mediated pyroptosis.
- To discuss its initiation, execution, and regulation.
- To highlight therapeutic strategies targeting pyroptosis.
Main Methods:
- Literature review of GSDM-mediated pyroptosis.
- Analysis of pyroptosis roles in physiological and pathological processes.
- Examination of programmed cell death crosstalk.
Main Results:
- GSDM proteins mediate pyroptosis in response to cellular stress.
- Pyroptosis releases inflammatory mediators, contributing to disease.
- Targeting pyroptotic pathways shows therapeutic potential.
Conclusions:
- GSDM-mediated pyroptosis is a critical inflammatory process.
- Dysregulation of pyroptosis contributes to various diseases.
- Developing drugs targeting pyroptosis is a promising therapeutic avenue.
Related Concept Videos
Pinching-off of Coated Vesicles
3.0K
Vesicle budding is orchestrated by distinct cytosolic proteins such as adaptor proteins, coat proteins, and GTPases. To initiate vesicle budding, membrane-bending proteins containing crescent-shaped BAR domains bind to the lipid heads in the bilayer and distort the membrane to form a protein-coated vesicle bud. Adaptors proteins such as AP2 for clathrin-coated vesicles can nucleate on the deformed membrane. Finally, coat proteins such as clathrin or COPI and COPII assemble into a coat forming...
3.0K
Actin Filament Depolymerization
3.0K
Actin filaments (F-actin) are composed of actin subunits. The dissociation of actin monomers can occur from either end of F-actin. The rate of dissociation is faster from the minus-end or the pointed end, where the actin subunits exist with a bound ADP, together known as ADP-actin. The depolymerization of F-actin is aided by proteins, including the actin-depolymerizing factor (ADF) and cofilin family of proteins, gelsolin, and glia maturation factor (GMF).
In F-actin, the ADF/cofilin proteins...
In F-actin, the ADF/cofilin proteins...
3.0K
Mechanical Protein Functions
4.9K
Proteins perform many mechanical functions in a cell. These proteins can be classified into two general categories- proteins that generate mechanical forces and proteins that are subjected to mechanical forces. Proteins providing mechanical support to the structure of the cell, such as keratin, are subjected to mechanical force, whereas proteins involved in cell movement and transport of molecules across cell membranes, such as an ion pump, are examples of generating mechanical force.
4.9K
Amplifying Signals via Enzymatic Cascade
8.2K
When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze...
8.2K
Overview of Cell Death
5.9K
Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
5.9K
Caspases
11.6K
Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
11.6K

