ArticleAging2019
β-arrestin-2 enhances intestinal epithelial apoptosis in necrotizing enterocolitis.
Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
The trial behind it
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Disruption of bile acid homeostasis potentiates Paneth cell ablation by activating the intestinal Farnesoid X receptor in necrotizing enterocolitis.NPJ biofilms and microbiomes · 2026Article
- GPCR systems coordinate cellular resilience against aging-associated stress.Frontiers in molecular biosciences · 2026Review
- GPCR Biased Signaling in Cancer.Handbook of experimental pharmacology · 2026Review
- β-arrestin2: an emerging player and potential therapeutic target in inflammatory immune diseases.Acta pharmacologica Sinica · 2025Review
- AntenatalInternational journal of molecular sciences · 2024Article
- Active polypeptide MDANP protect against necrotizing enterocolitis (NEC) by regulating the PERK-eIF2ɑ-QRICH1 axis.Scientific reports · 2023Article
- Probiotic supplementation attenuates age-related sarcopenia via the gut-muscle axis in SAMP8 mice.Journal of cachexia, sarcopenia and muscle · 2022Article
- Sulforaphane Ameliorates the Intestinal Injury in Necrotizing Enterocolitis by Regulating the PI3K/Akt/GSK-3Canadian journal of gastroenterology & hepatology · 2022Article
- HSPA5 Inhibitor Meliorate DSS-Induced Colitis through HSPA1A/CHIP.Disease markers · 2022Article
- Endoplasmic reticulum stress in the acute intestinal epithelial injury of necrotizing enterocolitis.Pediatric surgery international · 2021Review
- Differential Expression Profiles and Functional Prediction of circRNAs in Necrotizing Enterocolitis.BioMed research international · 2021Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis among intestinal epithelial cells contributes to necrotizing enterocolitis (NEC), a severe intestinal disease that particularly affects premature infants. β-arrestin-2, an important regulator of G-protein-coupled receptors, is expressed in intestinal epithelial cells, where its activation promotes apoptosis. We found that β-arrestin-2 was overexpressed in both human and murine NEC samples. β-arrestin-2-deficient mice were protected from endoplasmic reticulum stress and NEC development. The endoplasmic reticulum-resident chaperone BiP was found to promote intestinal epithelial cell survival. Pretreatment of intestinal epithelial cells or mice with the BiP inhibitor HA15 increased cell apoptosis and promoted NEC development. β-arrestin-2 bound to BiP and promoted its polyubiquitination and degradation, thereby facilitating the release of the pro-apoptotic molecule BIK from BiP. Silencing β-arrestin-2 downregulated apoptosis by increasing BiP levels, which suppressed endoplasmic reticulum stress. This study suggests that β-arrestin-2 induces NEC development by inhibiting BiP, thereby triggering apoptosis in response to endoplasmic reticulum stress. Thus, novel therapeutic strategies to inhibit β-arrestin-2 may enhance the treatment of NEC.
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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.