Evidence map›Paper›PMID 28004805›Full record

ArticleScientific reports2016

Tauroursodeoxycholic acid reduces ER stress by regulating of Akt-dependent cellular prion protein.

Yeo Min Yoon, Jun Hee Lee, Seung Pil Yun, Yong-Seok Han, Chul Won Yun, Hyun Jik Lee, Hyunjin Noh, Sei-Jung Lee, Ho Jae Han, Sang Hun Lee

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 3% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.

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  8. Pharmacological chaperones mitigate noise-induced hearing loss by attenuating sustained PERK activation.Proceedings of the National Academy of Sciences of the United States of America · 2026
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2 more citing papers are in PubMed but not listed here.

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

10 authors at 5 institutions in 2 countries.

Yeo Min YoonMedical Science Research Institute, Soonchunhyang University Seoul Hospital, Seoul, Republic of Korea.
Jun Hee LeeDepartment of Pharmacology and Toxicology, University of Alabama at Birmingham School of Medicine, Birmingham, AL 35294, USA.
Seung Pil YunNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, USA.
Yong-Seok HanMedical Science Research Institute, Soonchunhyang University Seoul Hospital, Seoul, Republic of Korea.
Chul Won YunMedical Science Research Institute, Soonchunhyang University Seoul Hospital, Seoul, Republic of Korea.
Hyun Jik LeeDepartment of Veterinary Physiology, College of Veterinary Medicine and Research Institute for Veterinary Science, and BK21 PLUS Creative Veterinary Research Center, Seoul National University, Seoul 151-741, Republic of Korea.
Hyunjin NohDepartment of Internal Medicine, Hyonam Kidney Laboratory, Soonchunhyang University, Seoul, Republic of Korea.
Sei-Jung LeeDepartment of Veterinary Physiology, College of Veterinary Medicine and Research Institute for Veterinary Science, and BK21 PLUS Creative Veterinary Research Center, Seoul National University, Seoul 151-741, Republic of Korea.
Ho Jae HanDepartment of Veterinary Physiology, College of Veterinary Medicine and Research Institute for Veterinary Science, and BK21 PLUS Creative Veterinary Research Center, Seoul National University, Seoul 151-741, Republic of Korea.
Sang Hun LeeMedical Science Research Institute, Soonchunhyang University Seoul Hospital, Seoul, Republic of Korea.
Soonchunhyang University Hospital · KRSeoul National University · KRJohns Hopkins University · USSoonchunhyang University · KRUniversity of Alabama at Birmingham · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although mesenchymal stem cells (MSCs) are a promising cell source for regenerative medicine, ischemia-induced endoplasmic reticulum (ER) stress induces low MSC engraftment and limits their therapeutic efficacy. To overcome this, we investigated the protective effect of tauroursodeoxycholic acid (TUDCA), a bile acid, on ER stress in MSCs in vitro and in vivo. In ER stress conditions, TUDCA treatment of MSCs reduced the activation of ER stress-associated proteins, including GRP78, PERK, eIF2α, ATF4, IRE1α, JNK, p38, and CHOP. In particular, TUDCA inhibited the dissociation between GRP78 and PERK, resulting in reduced ER stress-mediated cell death. Next, to explore the ER stress protective mechanism induced by TUDCA treatment, TUDCA-mediated cellular prion protein (PrP

Indexed as

AnimalsEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressHeterograftsHumansMaleMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMice, Inbred BALB CMice, NudeProto-Oncogene Proteins c-aktPrPC ProteinsSignal TransductionTaurochenodeoxycholic AcidEndoplasmic Reticulum Chaperone BiPHSPA5 protein, humanHspa5 protein, mouseProto-Oncogene Proteins c-aktPrPC ProteinsTaurochenodeoxycholic Acidursodoxicoltaurine

Identifiers

PMID28004805
PMCPMC5177936
OpenAlexW2562203536

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.