Evidence mapPaperPMID 34638652Full record

ReviewInternational journal of molecular sciences2021

Beta-Cell Dysfunction Induced by Tacrolimus: A Way to Explain Type 2 Diabetes?

Ana Elena Rodriguez-Rodriguez, Esteban Porrini, Armando Torres

Open access · goldAbstract readReview
In one paragraph

Review 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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

27 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. The therapeutic potential ofFrontiers in pharmacology · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Tacrolimus and diabetic rodent models.Pharmacological reports : PR · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Medication-Induced Hyperglycemia and Diabetes Mellitus: A Review of Current Literature and Practical Management Strategies.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2024
    Review
  15. International consensus on post-transplantation diabetes mellitus.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024
    Article
  16. Article
  17. Article
  18. Advanced therapy to cure diabetes: mission impossible is now possible?Frontiers in cell and developmental biology · 2024
    Review
  19. Review
  20. 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.

Ana Elena Rodriguez-RodriguezResearch Unit, Hospital Universitario de Canarias, 38320 La Laguna, Santa Cruz de Tenerife, Spain.ORCID 0000-0002-0803-864X
Esteban PorriniUnidad Ensayos Clinicos-UCICEC, Hospital Universitario de Canarias, 38320 La Laguna, Santa Cruz de Tenerife, Spain.
Armando TorresUnidad Ensayos Clinicos-UCICEC, Hospital Universitario de Canarias, 38320 La Laguna, Santa Cruz de Tenerife, Spain.
Universidad de La Laguna · ESHospital Universitario de Canarias · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The combination of insulin resistance and β-cells dysfunction leads to the onset of type-2 diabetes mellitus (T2DM). This process can last for decades, as β-cells are able to compensate the demand for insulin and maintain normoglycemia. Understanding the adaptive capacity of β-cells during this process and the causes of its failure is essential to the limit onset of diabetes. Post-transplant diabetes mellitus (PTDM) is a common and serious disease that affects 30% of renal transplant recipients. With the exception of immunosuppressive therapy, the risk factors for T2D are the same as for PTDM: obesity, dyslipidaemia, insulin resistance and metabolic syndrome. Tacrolimus (TAC) is the immunosuppressant of choice after renal transplantation but it has the highest rates of PTDM. Our group has shown that insulin resistance and glucolipotoxicity, without favouring the appearance of apoptosis, modify key nuclear factors for the maintenance of identity and functionality of β-cells. In this context, TAC accelerates or enhances these changes. Our hypothesis is that the pathways that are affected in the progression from pre-diabetes to diabetes in the general population are the same pathways that are affected by TAC. So, TAC can be considered a tool to study the pathogenesis of T2DM. Here, we review the common pathways of β-cells dysfunction on T2DM and TAC-induced diabetes.

Indexed as

AnimalsDiabetes Mellitus, Type 2HumansInsulin ResistanceInsulin-Secreting CellsKidney TransplantationTacrolimusTransplant RecipientsTacrolimusdiabetes mellitus type 2pancreatic β-cellspathwayspost-transplant diabetes mellitustacrolimus

Identifiers

PMID34638652
PMCPMC8509035
OpenAlexW3202679698

What Socratic 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 Socratic graph.