Evidence map›Paper›PMID 23076551›Full record

ReviewTransplantation2013

Calcineurin inhibition and new-onset diabetes mellitus after transplantation.

Harini A Chakkera, Lawrence J Mandarino

Open access · greenAbstract readReview
In one paragraph

Review in Transplantation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

44 citing papers in PubMed, 99 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Italian recommendations for the diagnosis and treatment of myasthenia gravis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Potential Antifungal Targets forInternational journal of molecular sciences · 2022
    Review
  18. 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

2 authors at 2 institutions in 1 country.

Harini A ChakkeraDivision of Nephrology and Hypertension, Mayo Clinic, Phoenix, AZ 85054, USA. chakkera.harini@mayo.edu
Lawrence J Mandarino
Mayo Clinic · USMayo Clinic in Florida · US

Funding

MOLECULAR REGULATION OF MUSCLE GLUCOSE METABOLISM IN MANR01DK047936 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI MANDARINO, LAWRENCE J · 1994 to 2022
$10.7M
PGC-1 & Muscle Mitochondrial Dysfunction in DiabetesR01DK066483 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI MANDARINO, LAWRENCE J · 2004 to 2018
$6.7M
NIDDK NIH HHS DK047936NIDDK NIH HHS DK066483NIDDK NIH HHS R01 DK047936NIDDK NIH HHS R01 DK066483
6 · The paper itself

Abstract

New-onset diabetes after transplantation independently increases the risk of cardiovascular disease, infections, and graft loss and decreases patient survival. The required balance between insulin sensitivity/resistance and insulin secretion is necessary to maintain normal glucose metabolism. Calcineurin inhibitors are standard immunosuppression drugs used after transplantation and have been implicated in the development of new-onset diabetes after transplantation partially by pancreatic β-cell apoptosis and resultant decrease in insulin secretion. The ability of muscle to take up glucose is critical to blood glucose homeostasis. Skeletal muscle is quantitatively the most important tissue in the body for insulin-stimulated glucose disposal and is composed of diverse myofibers that vary in their properties between healthy and insulin-resistant muscle. Various signaling pathways are responsible for remodeling of skeletal muscle, and among these is the calcineurin/nuclear factor of activated T-cell pathway. The mechanism of action of the calcineurin inhibitors is to bind in a complex with a binding protein to calcineurin and inhibit its dephosphorylation and activation of nuclear factor of activated T cells. In this review, we will provide a detailed discussion of the hypothesis that inhibition of calcineurin in tissues involved in insulin sensitivity/resistance could be at least partially responsible for the diabetogenicity seen with the use of calcineurin inhibitors.

Indexed as

Calcineurin InhibitorsAnimalsCalcineurinDiabetes MellitusGlucoseHumansImmunosuppressive AgentsInsulinInsulin ResistanceOrgan TransplantationCalcineurinCalcineurin InhibitorsGlucoseImmunosuppressive AgentsInsulin

Identifiers

PMID23076551
PMCPMC3884894
OpenAlexW2015132063

What OpenQuestion holds

Textmetadata
LicenceTDM
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.