Evidence map›Paper›PMID 33613564›Full record

ReviewFrontiers in immunology2020

A Concise Review on the Role of Endoplasmic Reticulum Stress in the Development of Autoimmunity in Vitiligo Pathogenesis.

Shahnawaz D Jadeja, Jay M Mayatra, Jayvadan Vaishnav, Nirali Shukla, Rasheedunnisa Begum

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Antioxidants (Basel, Switzerland) · 2023
    Article
  8. Leucoderma in Buffaloes (Animals : an open access journal from MDPI · 2023
    Article
  9. Review
  10. Review
  11. Role of HMGB1 in Vitiligo: Current Perceptions and Future Perspectives.Clinical, cosmetic and investigational dermatology · 2022
    Review
  12. Article
  13. 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

5 authors at 1 institution in 1 country.

Shahnawaz D JadejaDepartment of Biochemistry, Faculty of Science, The Maharaja Sayajirao University of Baroda, Vadodara, India.
Jay M MayatraDepartment of Biochemistry, Faculty of Science, The Maharaja Sayajirao University of Baroda, Vadodara, India.
Jayvadan VaishnavDepartment of Biochemistry, Faculty of Science, The Maharaja Sayajirao University of Baroda, Vadodara, India.
Nirali ShuklaDepartment of Biochemistry, Faculty of Science, The Maharaja Sayajirao University of Baroda, Vadodara, India.
Rasheedunnisa BegumDepartment of Biochemistry, Faculty of Science, The Maharaja Sayajirao University of Baroda, Vadodara, India.
Maharaja Sayajirao University of Baroda · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vitiligo is characterized by circumscribed depigmented macules in the skin resulting due to the autoimmune destruction of melanocytes from the epidermis. Both humoral as well as cell-mediated autoimmune responses are involved in melanocyte destruction. Several studies including ours have established that oxidative stress is involved in vitiligo onset, while autoimmunity contributes to the disease progression. However, the underlying mechanism involved in programing the onset and progression of the disease remains a conundrum. Based on several direct and indirect evidences, we suggested that endoplasmic reticulum (ER) stress might act as a connecting link between oxidative stress and autoimmunity in vitiligo pathogenesis. Oxidative stress disrupts cellular redox potential that extends to the ER causing the accumulation of misfolded proteins, which activates the unfolded protein response (UPR). The primary aim of UPR is to resolve the stress and restore cellular homeostasis for cell survival. Growing evidences suggest a vital role of UPR in immune regulation. Moreover, defective UPR has been implicated in the development of autoimmunity in several autoimmune disorders. ER stress-activated UPR plays an essential role in the regulation and maintenance of innate as well as adaptive immunity, and a defective UPR may result in systemic/tissue level/organ-specific autoimmunity. This review emphasizes on understanding the role of ER stress-induced UPR in the development of systemic and tissue level autoimmunity in vitiligo pathogenesis and its therapeutics.

Indexed as

AutoimmunityAdaptive ImmunityAnimalsEndoplasmic Reticulum StressHumansImmunity, InnateMelanocytesOxidative StressSignal TransductionSkinUnfolded Protein ResponseVitiligoautoimmunityendoplasmic reticulummelanocytesunfolded protein responsevitiligo

Identifiers

PMID33613564
PMCPMC7890234
OpenAlexW3126272417

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.