Evidence map›Paper›PMID 27913816›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2017

Genetic ablation or pharmacologic inhibition of autophagy mitigated NSAID-associated gastric damages.

Chan Young Ock, Jong-Min Park, Young-Min Han, Migyeong Jeong, Mi-Young Kim, Ho Jae Lee, Ki Baik Hahm

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 28% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Gut Microbiota in NSAID Enteropathy: New Insights From Inside.Frontiers in cellular and infection microbiology · 2021
    Review
  5. Review
  6. Article
  7. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Chan Young OckDepartment of Internal Medicine, Seoul National University Hospital, Seoul, 110-744, South Korea.
Jong-Min ParkCHA Cancer Prevention Research Center, CHA Bio Complex and Digestive Disease Center, CHA University Bundang Medical Center, 59 Yatap-ro, Bundang-gu, Seongnam, 463-712, South Korea.
Young-Min HanCHA Cancer Prevention Research Center, CHA Bio Complex and Digestive Disease Center, CHA University Bundang Medical Center, 59 Yatap-ro, Bundang-gu, Seongnam, 463-712, South Korea.
Migyeong JeongCHA Cancer Prevention Research Center, CHA Bio Complex and Digestive Disease Center, CHA University Bundang Medical Center, 59 Yatap-ro, Bundang-gu, Seongnam, 463-712, South Korea.
Mi-Young KimDigestive Disease Center, CHA University Bundang Medical Center, Seongnam, 460-740, South Korea.
Ho Jae LeeLaboratory of Chemoprevention, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon, 406-740, South Korea.
Ki Baik HahmCHA Cancer Prevention Research Center, CHA Bio Complex and Digestive Disease Center, CHA University Bundang Medical Center, 59 Yatap-ro, Bundang-gu, Seongnam, 463-712, South Korea. hahmkb@cha.ac.kr.
CHA University · KRGachon University · KRSeoul National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-steroidal anti-inflammatory drug (NSAID)-associated endoplasmic reticulum (ER) stress (a cyclooxygenase-2-independent mechanism) and consequent autophagic cell death are responsible for NSAID-associated gastric damage. Therefore, alleviating cytotoxicity executed via ER stress and autophagy can be a strategy to prevent NSAID-associated gastric damage. Here, we explored whether genetic or pharmacologic inhibition of autophagy can mitigate NSAID-associated gastric damage in in vitro and in vivo models. To examine the effects of genetic inhibition of NSAID-associated autophagy, we administered indomethacin to RGM1 gastric mucosal cells transfected with shPERK, siLC3B, or shATG5 and microtubule-associated protein light chain 3B knock-out (LC3B KEY MESSAGES: NSAID administration triggered ER stress and subsequent autophagy. Inhibition of autophagy resulted in attenuated NSAID-associated cytotoxicity. Autophagy inhibitors represent a novel strategy to prevent NSAID-associated gastric damage.

Indexed as

AdenineAnimalsAnti-Inflammatory Agents, Non-SteroidalAutophagyCell LineChloroquineEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressGastric MucosaHumansIndomethacinMaleMicrotubule-Associated ProteinsProtective AgentsRats, Inbred WKYRNA Interference3-methyladenineAdenineAnti-Inflammatory Agents, Non-SteroidalChloroquineEndoplasmic Reticulum Chaperone BiPHSPA5 protein, humanHspa5 protein, mouseIndomethacinMap1lc3b protein, mouseMicrotubule-Associated ProteinsProtective Agents3-MAApoptosisAutophagy inhibitionChloroquineER stressGastric damagesLC3B knock-outNSAIDRescue

Identifiers

PMID27913816
OpenAlexW2559586979

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.