Evidence map›Paper›PMID 29986432›Full record

ArticleInternational journal of molecular sciences2018

Effect of Endoplasmic Reticular Stress on Free Hemoglobin Metabolism and Liver Injury.

Sung-Hui Tseng, Ting-Yun Chang, Chun-Kuang Shih, Rong-Hong Hsieh, Chia-Wen Chen, Yi-Chun Chen, Mei-Hsiang Lin, Jung-Su Chang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 54% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. 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

8 authors at 2 institutions in 1 country.

Sung-Hui TsengDepartment of Physical Medicine and Rehabilitation, Taipei Medical University Hospital, Taipei 110, Taiwan. m003089010@tmu.edu.tw.
Ting-Yun ChangSchool of Nutrition and Health Sciences, College of Nutrition, Taipei Medical University, Taipei 110, Taiwan. soul0528@hotmail.com.tw.
Chun-Kuang ShihSchool of Nutrition and Health Sciences, College of Nutrition, Taipei Medical University, Taipei 110, Taiwan. ckshih@tmu.edu.tw.
Rong-Hong HsiehSchool of Nutrition and Health Sciences, College of Nutrition, Taipei Medical University, Taipei 110, Taiwan. hsiehrh@tmu.edu.tw.
Chia-Wen ChenSchool of Nutrition and Health Sciences, College of Nutrition, Taipei Medical University, Taipei 110, Taiwan. d301091008@tmu.edu.tw.
Yi-Chun ChenSchool of Nutrition and Health Sciences, College of Nutrition, Taipei Medical University, Taipei 110, Taiwan. yichun@tmu.edu.tw.ORCID 0000-0002-6930-1712
Mei-Hsiang LinDepartment of Pharmaceutical Science, School of Pharmacy, Taipei Medical University, Taipei 110, Taiwan. mhl00001@tmu.edu.tw.
Jung-Su ChangSchool of Nutrition and Health Sciences, College of Nutrition, Taipei Medical University, Taipei 110, Taiwan. susanchang@tmu.edu.tw.
Taipei Medical University · TWTaipei Medical University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elevated soluble (s) CD163 and free hemoglobin (Hb) levels predict fatty liver progression; however, the molecular mechanisms underlying Hb metabolism and liver injury remain undefined. We investigated the effects of endoplasmic reticular (ER) stress on red blood cell (RBC) rheology and free Hb recycling pathways. ER stress was induced in Sprague-Dawley rats by an intraperitoneal injection of tunicamycin (TM) (50, 100, and 200 μg/100 g body weight (BW)) or an intravenous injection of Hb (5 mg/100 g BW). A TM injection increased sCD163 levels, attenuated free Hb uptake, and maintained RBC aggregability. An Hb injection increased serum LVV-hemorphin-7 and total bilirubin levels, but this effect was suppressed by TM. A Western blot analysis showed that ER stress suppressed Hb degradation in the liver through downregulation of globin degradation proteins cathepsin D and glyoxalase-1, as well as heme degradation protein heme oxyganase-1 and keap-1 expression. An ER stress activator also increased the translocation of nuclear factor (NF)-κB (p65) and nuclear factor-erythroid 2-related factor 2 (Nrf2) to nuclei. In conclusion, ER stress triggers ineffective Hb metabolism via altering globin and heme iron degradation pathways. Inability to recycle and metabolize free Hb may underlie the association between iron dysfunction and liver injury.

Indexed as

AnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticBilirubinCathepsin DCD163 AntigenEndoplasmic Reticulum StressErythrocytesHemeHemoglobinsInjections, IntraperitonealInjections, IntravenousIronLactoylglutathione LyaseLiverMaleAntigens, CDAntigens, Differentiation, MyelomonocyticBilirubinCathepsin DCD163 AntigenCtsd protein, ratGLO1 protein, humanHemeHemoglobinsIronLactoylglutathione LyaseLVV-hemorphin-7Peptide FragmentsReceptors, Cell SurfaceTunicamycinendoplasmic reticular stressfree hemoglobinliver injurysoluble (s) CD163

Identifiers

PMID29986432
PMCPMC6073154
OpenAlexW2817277080

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.