Related Experiment Video

Updated: Sep 2, 2025

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
06:52

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages

Published on: May 21, 2018

10.8K

Targeting autophagy regulation in NLRP3 inflammasome-mediated lung inflammation in COVID-19

Yuan-Yuan Yong1, Li Zhang1, Yu-Jiao Hu2

  • 1Sichuan Key Medical Laboratory of New Drug Discovery and Druggability Evaluation, Materia Medica, Luzhou Key Laboratory of Activity Screening and Druggability Evaluation for Chinese Materia Medica, School of Pharmacy; Education Ministry Key Laboratory of Medical Electrophysiology, School of Preclinical Medicine, Southwest Medical University, Luzhou 646000, China.

Clinical Immunology (Orlando, Fla.)
|August 9, 2022
PubMed

Insights

Autophagy regulates SARS-CoV-2 infection and NLRP3 inflammasome activation in COVID-19. Autophagy activators show therapeutic potential by inhibiting the NLRP3 inflammasome and cytokine storm.

Area of Science:

  • Immunology
  • Cell Biology
  • Virology

Background:

  • COVID-19, caused by SARS-CoV-2, involves NLRP3 inflammasome activation leading to cytokine storms.
  • Autophagy plays a dual role in SARS-CoV-2 infection, impacting viral replication and inflammation.

Purpose of the Study:

  • To review autophagy regulation in COVID-19 pathogenesis.
  • To highlight the therapeutic potential of autophagy activators in managing COVID-19.

Main Methods:

  • Literature review focusing on autophagy and NLRP3 inflammasome in COVID-19.
  • Analysis of the interplay between autophagy, SARS-CoV-2, and inflammasome activation.

Main Results:

  • Autophagy modulates SARS-CoV-2 early-stage infection and replication.
  • NLRP3 inflammasome activation drives late-stage inflammation and cytokine storm in COVID-19.
  • Autophagy activators can inhibit NLRP3 inflammasome-mediated lung inflammation.

Conclusions:

  • Autophagy modulation is crucial at different stages of COVID-19.
  • Targeting autophagy, particularly with activators, offers a promising strategy to mitigate cytokine storms.
  • Combination therapies involving autophagy modulators and NLRP3 inhibitors, antivirals, or anti-inflammatories warrant further investigation.
Keywords:
Autophagy regulationCOVID-19Lung inflammationNLRP3 inflammasomeSARS-CoV-2

More Related Videos

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells09:04

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells

Published on: May 22, 2014

21.0K
Evaluation of Caspase Activation to Assess Innate Immune Cell Death10:23

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

3.3K

Related Concept Videos

Autophagy01:27

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
4.5K
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
7.8K
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
3.5K
Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
2.6K
Delivery Pathways to the Lysosome01:36

Delivery Pathways to the Lysosome

Eukaryotic cells use different mechanisms to eliminate toxic waste obsolete and worn-out substances. Lysosomes play a pivotal role in this, and hence, these substances are carried to the lysosome from other parts of the cell and extracellular space through different pathways. The most elaborately studied pathways to the lysosome are the endocytic pathways.
Endocytosis
In endocytosis, the cell membrane takes up macromolecules and particles from the surrounding medium. Clathrin-mediated...
6.7K
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
3.0K