Evidence map›Paper›PMID 33599437›Full record

ReviewPediatric endocrinology, diabetes, and metabolism2021

β-cell self-destruction and extremely complicated and still unknown etiopathogenesis of type 1 diabetes.

Artur Chwalba, Aleksandra Pilśniak, Ewa Otto-Buczkowska

Open access · diamondAbstract readReview
In one paragraph

Review in Pediatric endocrinology, diabetes, and metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Ginsenoside Rg1 Ameliorates Pancreatic Injuries via the AMPK/mTOR Pathway in vivo and in vitro.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023
    Article
  3. Article
  4. Article
  5. 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

3 authors at 2 institutions in 1 country.

Artur ChwalbaDepartment of Pharmacology, Medical University of Silesia, Poland.
Aleksandra PilśniakInpatient Department of Radiation and Clinical Oncology, Maria Skłodowska-Curie Institute - Oncology Center, Gliwice Branch, Poland.
Ewa Otto-BuczkowskaMedical Specialist Centre in Gliwice, Medical Specialist Centre in Gliwice, Poland.
The Maria Sklodowska-Curie National Research Institute of Oncology · PLMedical University of Silesia · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes is based on apoptosis, which leads to b-cell death. Factors triggering apoptosis processes are very diverse and currently not fully explained. The main role is attributed to genetic and environmental factors. Genetic studies have shown that the inherited propensity for type 1 diabetes is multi-genetic. Environmental factors modify the response to their own antigens, but are probably not necessary to start the autoaggression process. The effect of b-cell destruction is confirmed by the appearance of autoantibodies in the blood. The paper presents a review of the available literature regarding the self-destruction of pancreatic b-cells. The aim of the study was to draw attention to the extremely complicated and still unknown etiopathogenesis of type 1 diabetes by reviewing current literature related to the above topic. The goal is to acquire the knowledge necessary to develop and implement causal treatment for diabetes. At the moment, unfortunately, we do not have safe, innovative therapy methods in the field of diabetes prevention. Intensive research on the etiopathogenesis of type 1 diabetes is an extremely important field of medical research.

Indexed as

Diabetes Mellitus, Type 1Insulin-Secreting CellsAutoantibodiesHumansAutoantibodiesapoptosisautoantibodiesb-cell destructionimmunological markers.type 1 diabetes

Identifiers

PMID33599437
PMCPMC10227476
OpenAlexW3126535292

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.