ArticleBMB reports2021
Autophagy down-regulates NLRP3-dependent inflammatory response of intestinal epithelial cells under nutrient deprivation.
Article in BMB reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- BECN1 Protects Against Intestinal Ischemia/Reperfusion Injury by Promoting NLRP3 Ubiquitination and Suppressing Inflammasome Activation.Digestive diseases and sciences · 2026Article
- Targeted autophagy: research progress on the regulatory potential of periodontitis prevention and treatment.Frontiers in cell and developmental biology · 2026Review
- A20 Attenuates Inflammatory Injury in Bovine Endometrial Epithelial Cells Through Autophagy-Mediated NLRP3 Inflammasome Inactivation.Animals : an open access journal from MDPI · 2025Article
- Dysregulation of autophagy during photoaging reduce oxidative stress and inflammatory damage caused by UV.Frontiers in pharmacology · 2025Review
- Article
- Autophagy in colitis-associated colon cancer: exploring its potential role in reducing initiation and preventing IBD-Related CAC development.Autophagy · 2024Review
- Spermidine-Eugenol Supplement Preserved Inflammation-Challenged Intestinal Cells by Stimulating Autophagy.International journal of molecular sciences · 2023Article
- Effects of dietaryFrontiers in immunology · 2023Article
- Corilagin alleviates intestinal ischemia/reperfusion-induced intestinal and lung injury in miceFrontiers in pharmacology · 2022Article
- NLRP3 Inflammasome: Checkpoint Connecting Innate and Adaptive Immunity in Autoimmune Diseases.Frontiers in immunology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulation of inflammation induced by noninfectious stress conditions, such as nutrient deprivation, causes tissue damage and intestinal permeability, resulting in the development of inflammatory bowel diseases. We studied the effect of autophagy on cytokine secretion related to intestinal permeability under nutrient deprivation. Autophagy removes NLRP3 inflammasomes via ubiquitin-mediated degradation under starvation. When autophagy was inhibited, starvation-induced NLRP3 inflammasomes and their product, IL-1β, were significantly enhanced. A prolonged nutrient deprivation resulted in an increased epithelial mesenchymal transition (EMT), leading to intestinal permeability. Under nutrient deprivation, IL-17E/25, which is secreted by IL-1β, demolished the intestinal epithelial barrier. Our results suggest that an upregulation of autophagy maintains the intestinal barrier by suppressing the activation of NLRP3 inflammasomes and the release of their products, including proinflammatory cytokines IL-1β and IL-17E/25, under nutrient deprivation. [BMB Reports 2021; 54(5): 260-265].
Indexed as
Identifiers
33407996PMC8167250W3120602598What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.