Evidence map›Paper›PMID 35402506›Full record

ReviewFrontiers in molecular biosciences2022

Endoplasmic Reticulum Stress of Gut Enterocyte and Intestinal Diseases.

Han Gao, Chengwei He, Rongxuan Hua, Yuexin Guo, Boya Wang, Chen Liang, Lei Gao, Hongwei Shang, Jing-Dong Xu

Erratum issuedOpen access · goldAbstract readReview
In one paragraph

Review in Frontiers in molecular biosciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Mitochondria-Homing Drug Mitochonic Acid 5 Improves Barth Syndrome Myopathy in a Human-Induced Pluripotent Stem Cell Model and Barth Syndrome Drosophila Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  7. Article
  8. Article
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  11. Investigation of the mutual crosstalk between ER stress and PI3K/AKT/mTOR signaling pathway in iron overload-induced liver injury in chicks.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024
    Article
  12. Article
  13. Article
  14. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Han GaoDepartment of Physiology and Pathophysiology, Basic Medical College, Capital Medical University, Beijing, China.
Chengwei HeDepartment of Physiology and Pathophysiology, Basic Medical College, Capital Medical University, Beijing, China.
Rongxuan HuaDepartment of Clinical Medicine, Basic Medical College, Capital Medical University, Beijing, China.
Yuexin GuoDepartment of Oral Medicine, Basic Medical College, Capital Medical University, Beijing, China.
Boya WangUndergraduate Student of 2018 Eight Program of Clinical Medicine, Peking University Health Science Center, Beijing, China.
Chen LiangDepartment of Clinical Medicine, Basic Medical College, Capital Medical University, Beijing, China.
Lei GaoDepartment of Biomedical Informatics, School of Biomedical Engineering, Capital Medical University, Beijing, China.
Hongwei ShangExperimental Center for Morphological Research Platform, Capital Medical University, Beijing, China.
Jing-Dong XuDepartment of Physiology and Pathophysiology, Basic Medical College, Capital Medical University, Beijing, China.
Capital Medical University · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The endoplasmic reticulum, a vast reticular membranous network from the nuclear envelope to the plasma membrane responsible for the synthesis, maturation, and trafficking of a wide range of proteins, is considerably sensitive to changes in its luminal homeostasis. The loss of ER luminal homeostasis leads to abnormalities referred to as endoplasmic reticulum (ER) stress. Thus, the cell activates an adaptive response known as the unfolded protein response (UPR), a mechanism to stabilize ER homeostasis under severe environmental conditions. ER stress has recently been postulated as a disease research breakthrough due to its significant role in multiple vital cellular functions. This has caused numerous reports that ER stress-induced cell dysfunction has been implicated as an essential contributor to the occurrence and development of many diseases, resulting in them targeting the relief of ER stress. This review aims to outline the multiple molecular mechanisms of ER stress that can elucidate ER as an expansive, membrane-enclosed organelle playing a crucial role in numerous cellular functions with evident changes of several cells encountering ER stress. Alongside, we mainly focused on the therapeutic potential of ER stress inhibition in gastrointestinal diseases such as inflammatory bowel disease (IBD) and colorectal cancer. To conclude, we reviewed advanced research and highlighted future treatment strategies of ER stress-associated conditions.

Indexed as

cell deathcolon cancerendoplasmic reticulum stressinflammatory bowel diseasetreatment targetunfolded protein response

Identifiers

PMID35402506
PMCPMC8988245
OpenAlexW4221034998

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.