Evidence map›Paper›PMID 33651226›Full record

ArticleCell biology and toxicology2021

Inhibition of ER stress attenuates kidney injury and apoptosis induced by 3-MCPD via regulating mitochondrial fission/fusion and Ca

Yujie Zhong, Chengni Jin, Jiahui Han, Jiachang Zhu, Qi Liu, Dianjun Sun, Xiaodong Xia, Xiaoli Peng

Abstract read
PubMed Publisher
In one paragraph

Article in Cell biology and toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Angiotensin-(1-9) prevents angiotensin II-induced endothelial apoptosis through CNPY2/PERK pathway.Apoptosis : an international journal on programmed cell death · 2023
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

8 authors at 2 institutions in 1 country.

Yujie ZhongCollege of Food Science and Engineering, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Chengni JinCollege of Food Science and Engineering, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Jiahui HanCollege of Food Science and Engineering, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Jiachang ZhuCollege of Food Science and Engineering, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Qi LiuCollege of Food Science and Engineering, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Dianjun SunCollege of Food Science and Engineering, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Xiaodong XiaCollege of Food Science and Engineering, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Xiaoli PengCollege of Food Science and Engineering, Northwest A&F University, Yangling, 712100, Shaanxi, China. pxlpxh@163.com.ORCID 0000-0003-3676-892X
Northwest A&F University · CNNorth West Agriculture and Forestry University · CN

Funding

National Natural Science Foundation of China 31571928Science and Technology Plan Project of Shaanxi Province 2020NY-106Student's Platform for Innovation and Entrepreneurship Training Program 1201710712149, 1201710712127
6 · The paper itself

Abstract

3-Chloro-1, 2-propanediol (3-MCPD) is a food-borne toxic substance well-known for more than 40 years that is mainly associated with nephrotoxicity. A better understanding of 3-MCPD nephrotoxicity is required to devise efficacious strategies to counteract its toxicity. In the present work, the role of endoplasmic reticulum (ER) stress along with its underlying regulatory mechanism in 3-MCPD-mediated renal cytotoxicity was investigated in vivo and in vitro. Our data indicated that 3-MCPD-stimulated ER stress response evidenced by sustained activation of PERK-ATF4-p-CHOP and IRE1 branches in Sprague Dawley (SD) rats and human embryonic kidney (HEK293) cells. Moreover, ER stress-associated specific apoptotic initiator, caspase 12, was over-expressed. Blocking ER stress with its antagonist, 4-phenylbutyric acid (4-PBA), improved the morphology and function of kidney effectively. 4-PBA also increased cell viability, relieved mitochondrial vacuolation, and inhibited cell apoptosis through regulating caspase-dependent intrinsic apoptosis pathways. Furthermore, the enhanced expressions of two mitochondrial fission proteins, DRP1/p-DRP1 and FIS1, and the relocation of DRP1 on mitochondria subjected to 3-MPCD were reversed by 4-PBA, while the expression of the fusion protein, MFN2, was restored. Moreover, cellular Ca

Indexed as

alpha-ChlorohydrinMitochondrial DynamicsAnimalsApoptosisCalcium-Calmodulin-Dependent Protein Kinase KinaseEndoplasmic Reticulum StressHEK293 CellsHomeostasisHumansKidneyRatsRats, Sprague-Dawleyalpha-ChlorohydrinCalcium-Calmodulin-Dependent Protein Kinase KinaseCAMKK2 protein, human3-MCPD4-PBAApoptosisEndoplasmic reticulum stressKidneyMitochondrion

Identifiers

PMID33651226
OpenAlexW3134035843

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.