What question did this study set out to answer?

To elucidate the regulatory mechanisms of mTOR-dependent autophagy via TLR4-MyD88-MAPK and NF-κB pathways and evaluate its therapeutic potential in intestinal inflammation and oxidative injury.

August 29, 2018EBioMedicineOpen Access

Boosting mTOR-dependent autophagy via upstream TLR4-MyD88-MAPK signalling and downstream NF-κB pathway quenches intestinal inflammation and oxidative stress injury

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To elucidate the regulatory mechanisms of mTOR-dependent autophagy via TLR4-MyD88-MAPK and NF-κB pathways and evaluate its therapeutic potential in intestinal inflammation and oxidative injury.
Assessed upstream TLR4-MyD88-MAPK signaling and downstream NF-κB pathway activity in the regulation of mTOR-dependent autophagy.
Evaluated the impact of pathway modulation on intestinal inflammation and oxidative stress injury.
Upregulation of mTOR-dependent autophagy alleviated intestinal inflammation and mitigated oxidative stress injury.
Signaling modulation illuminated prospective therapeutic targets for managing refractory inflammatory bowel disease.

Implication

Preclinical study demonstrates enhanced mTOR-dependent autophagy suppresses intestinal inflammation, indicating novel targets for inflammatory bowel disease.

Abstract

Our findings not only shed light on the regulatory mechanism of mTOR-dependent autophagy, but also provided potential therapeutic targets for intestinal inflammatory diseases such as refractory inflammatory bowel disease.

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Cite This Study

Zhou et al. (2018) studied this question.

synapsesocial.com/papers/69d990492a25b240b7a3ce77 https://doi.org/10.1016/j.ebiom.2018.08.035

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Implication

Preclinical study demonstrates enhanced mTOR-dependent autophagy suppresses intestinal inflammation, indicating novel targets for inflammatory bowel disease.

Boosting mTOR-dependent autophagy via upstream TLR4-MyD88-MAPK signalling and downstream NF-κB pathway quenches intestinal inflammation and oxidative stress injury

Key Points

Implication

Abstract

Discussion

Cite This Study

Boosting mTOR-dependent autophagy via upstream TLR4-MyD88-MAPK signalling and downstream NF-κB pathway quenches intestinal inflammation and oxidative stress injury

Key Points

Implication

Abstract

Discussion

Cite This Study

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