Evidence map›Paper›PMID 34681610›Full record

ArticleInternational journal of molecular sciences2021

Selective Activation of Endoplasmic Reticulum Stress by Reactive-Oxygen-Species-Mediated Ochratoxin A-Induced Apoptosis in Tubular Epithelial Cells.

Chong-Sun Khoi, Yu-Wen Lin, Jia-Huang Chen, Biing-Hui Liu, Tzu-Yu Lin, Kuan-Yu Hung, Chih-Kang Chiang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. 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
2.2field-weighted citation impact, top 12% 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, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Tumor necrosis factor α-induced endoplasmic reticulum stress promotes airway smooth muscle cell proliferation.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. Review
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.

Chong-Sun KhoiGraduate Institute of Toxicology, College of Medicine, National Taiwan University, Taipei 10617, Taiwan.ORCID 0000-0003-1040-9857
Yu-Wen LinGraduate Institute of Toxicology, College of Medicine, National Taiwan University, Taipei 10617, Taiwan.
Jia-Huang ChenGraduate Institute of Toxicology, College of Medicine, National Taiwan University, Taipei 10617, Taiwan.ORCID 0000-0003-2879-7624
Biing-Hui LiuGraduate Institute of Toxicology, College of Medicine, National Taiwan University, Taipei 10617, Taiwan.
Tzu-Yu LinDepartment of Anesthesiology, Far-Eastern Memorial Hospital, New Taipei City 22060, Taiwan.
Kuan-Yu HungDepartment of Internal Medicine, College of Medicine and Hospital, National Taiwan University, Taipei 10617, Taiwan.
Chih-Kang ChiangGraduate Institute of Toxicology, College of Medicine, National Taiwan University, Taipei 10617, Taiwan.ORCID 0000-0001-9021-4616
National Taiwan University · TWFar Eastern Memorial Hospital · TWNational Taiwan University Hospital · TW

Funding

Far-Eastern Memorial Hospital 108-FTN16Ministry of Science and Technology, Taiwan MOST-107-2314-B-002-027-MY3Ministry of Science and Technology, Taiwan MOST- 110-2314-B-002 -130National Taiwan University Hospital 108-FTN16National Taiwan University Hospital NTUH- 108-S4373National Taiwan University Hospital NTUH-110-S5074National Taiwan University Hospital NTUH-UN-109-S4785
6 · The paper itself

Abstract

Ochratoxin A (OTA), one of the major food-borne mycotoxins, impacts the health of humans and livestock by contaminating food and feed. However, the underlying mechanism of OTA nephrotoxicity remains unknown. This study demonstrated that OTA induced apoptosis through selective endoplasmic reticulum (ER) stress activation in human renal proximal tubular cells (HK-2). OTA increased ER-stress-related JNK and precursor caspase-4 cleavage apoptotic pathways. Further study revealed that OTA increased reactive oxygen species (ROS) levels, and N-acetyl cysteine (NAC) could reduce OTA-induced JNK-related apoptosis and ROS levels in HK-2 cells. Our results demonstrate that OTA induced ER stress-related apoptosis through an ROS-mediated pathway. This study provides new evidence to clarify the mechanism of OTA-induced nephrotoxicity.

Indexed as

ApoptosisCell Cycle CheckpointsCell LineCell SurvivalEndoplasmic Reticulum StressEndoribonucleasesEpithelial CellsHumansJNK Mitogen-Activated Protein KinasesKidney Tubules, ProximalOchratoxinsOxidative StressProtein Serine-Threonine KinasesReactive Oxygen SpeciesEndoribonucleasesERN1 protein, humanJNK Mitogen-Activated Protein Kinasesochratoxin AOchratoxinsProtein Serine-Threonine KinasesReactive Oxygen SpeciesapoptosisER stressHK-2 cellochratoxin Areactive oxygen species

Identifiers

PMID34681610
PMCPMC8535626
OpenAlexW3205862158

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.