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Inflammation

Inflammation

The JAK-STAT Signaling Pathway

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...

Interactions Between Signaling Pathways

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...

Nitric Oxide Signaling Pathway

Nitric Oxide Signaling Pathway

Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...

Intracellular Signaling Cascades

Intracellular Signaling Cascades

Once a ligand binds to a receptor, the signal is transmitted through the membrane and into the cytoplasm. The continuation of a signal in this manner is called signal transduction. Signal transduction only occurs with cell-surface receptors, which cannot interact with most components of the cell, such as DNA. Only internal receptors can interact directly with DNA in the nucleus to initiate protein synthesis. When a ligand binds to its receptor, conformational changes occur that affect the...

Amplifying Signals via Second Messengers

Amplifying Signals via Second Messengers

Many receptor binding ligands are hydrophilic; they do not cross the cell membrane but bind to cell-surface receptors. Thus, their message must be relayed by second messengers present in the cell cytoplasm. There are several second messenger pathways, each with its own way of relaying information. For example, the G protein-coupled receptors can activate both phosphoinositol and cyclic AMP (cAMP) second messenger pathways. The phosphoinositol pathway is active when the receptor induces...

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Related Experiment Video

Updated: May 14, 2025

Implantation of a Carotid Cuff for Triggering Shear-stress Induced Atherosclerosis in Mice

Implantation of a Carotid Cuff for Triggering Shear-stress Induced Atherosclerosis in Mice

Published on: January 13, 2012

The cGAS-STING pathway in atherosclerosis.

Si-Yu Wang^1,2,3, Yu-Shan Chen^1,2, Bo-Yuan Jin^1,2,3

¹Heart Center/National Regional (Traditional Chinese Medicine) Cardiovascular Diagnosis and Treatment Center, The First Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, Henan, China.

Frontiers in Cardiovascular Medicine

|May 12, 2025

Summary

The cGAS-STING pathway drives atherosclerosis (AS) by promoting inflammation. Inhibiting this pathway offers a promising strategy to treat cardiovascular diseases (CVD).

Keywords:

STING inhibitors atherosclerosis cGAS inhibitors cGAS-STING pathway risk factors therapeutic potential

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Last Updated: May 14, 2025

Implantation of a Carotid Cuff for Triggering Shear-stress Induced Atherosclerosis in Mice

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Published on: January 13, 2012

Site Specific Lysine Acetylation of Histones for Nucleosome Reconstitution using Genetic Code Expansion in Escherichia coli

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Published on: December 26, 2020

A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites

A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites

Published on: August 8, 2014

Area of Science:

Immunology
Cardiovascular Science
Molecular Biology

Background:

Atherosclerosis (AS) is a chronic inflammatory disease and a major cause of cardiovascular morbidity and mortality.
The cGAS-STING pathway, an innate immune signaling cascade, is increasingly recognized for its role in AS progression.
Risk factors for AS may amplify the cGAS-STING pathway, exacerbating inflammation.

Purpose of the Study:

To review the mechanisms of the cGAS-STING pathway.
To explore the role of the cGAS-STING pathway in atherosclerosis.
To evaluate potential therapeutic inhibitors targeting the cGAS-STING pathway for cardiovascular diseases (CVD).

Main Methods:

Literature review of studies on the cGAS-STING pathway and atherosclerosis.
Analysis of the molecular mechanisms underlying cGAS-STING pathway activation in AS.
Evaluation of preclinical and clinical data on cGAS-STING inhibitors.

Main Results:

The cGAS-STING pathway is activated by cytoplasmic DNA, leading to inflammation and plaque formation in AS.
Established AS risk factors may potentiate cGAS-STING signaling, amplifying inflammatory responses.
Several inhibitors targeting the cGAS-STING pathway show therapeutic potential.

Conclusions:

The cGAS-STING pathway is a critical mediator of inflammation in atherosclerosis.
Targeting the cGAS-STING pathway presents a novel therapeutic avenue for AS and associated CVD.
Further research into cGAS-STING inhibitors could lead to effective treatments for cardiovascular diseases.