Evidence map›Paper›PMID 33225712›Full record

ReviewAmerican journal of physiology. Renal physiology2021

Calcineurin inhibitors: a double-edged sword.

Adaku C Ume, Tara-Yesomi Wenegieme, Clintoria R Williams

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
0.8field-weighted citation impact, top 28% 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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Ethyl acetate fraction ofJournal of traditional and complementary medicine · 2026
    Article
  5. Tenofovir, Interferon Pathways, and Mucosal Immunity: Implications for People Living With HIV.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026
    Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Neurotoxicity of Calcineurin Inhibitors.Annals of Indian Academy of Neurology · 2025
    Article
  12. TNF inhibits NKCC2 phosphorylation by a calcineurin-dependent pathway.American journal of physiology. Renal physiology · 2025
    Article
  13. Review
  14. Article
  15. Unlocking Transplant Tolerance with Biomaterials.Advanced healthcare materials · 2025
    Review
  16. Review
  17. Review
  18. Article
  19. Article
  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 1 institution in 1 country.

Adaku C UmeDepartment of Neuroscience Cell Biology and Physiology, Boonshoft School of Medicine, College of Science and Mathematics, Wright State University, Dayton, Ohio.ORCID 0000-0003-0219-8172
Tara-Yesomi WenegiemeDepartment of Neuroscience Cell Biology and Physiology, Boonshoft School of Medicine, College of Science and Mathematics, Wright State University, Dayton, Ohio.
Clintoria R WilliamsDepartment of Neuroscience Cell Biology and Physiology, Boonshoft School of Medicine, College of Science and Mathematics, Wright State University, Dayton, Ohio.
Wright State University · US

Funding

Role of Calcineurin Isoforms in Renal Regulation of Blood PressureR21DK119879 · NIDDK · WRIGHT STATE UNIVERSITY · PI WILLIAMS, CLINTORIA RICHARDS · 2018 to 2020
$630k
NIDDK NIH HHS R21 DK119879
6 · The paper itself

Abstract

Recently, research has directed its interests into identifying molecular pathways implicated in calcineurin inhibitor (CNI)-induced renal fibrosis. An emerging body of studies investigating calcineurin (CnA) activity has identified distinct actions of two main ubiquitously expressed isoforms: CnAα and CnAβ. CNIs have the capacity to inhibit both of these CnA isoforms. In the kidney, CnAα is required for development, whereas CnAβ predominantly modulates the immune response and glomerular hypertrophic signaling powered by activation of the transcription factor, nuclear factor of activated T lymphocytes (NFAT). Interestingly, data have shown that loss of CnAα activity contributes to the expression of profibrotic proteins in the kidney. Although this finding is of great significance, follow-up studies are needed to identify how loss of the CnAα isoform causes progressive renal damage. In addition, it is also necessary to identify downstream mediators of CnAα signaling that assist in upregulation of these profibrotic proteins. The goal of this review is to provide insight into strides taken to close the gap in elucidating CnA isoform-specific mechanisms of CNI-induced renal fibrosis. It is with hope that these contributions will lead to the development of newer generation CNIs that effectively blunt the immune response while circumventing extensive renal damage noted with long-term CNI use.

Indexed as

AnimalsCalcineurinCalcineurin InhibitorsFibrosisHumansImmunosuppressive AgentsKidneyKidney DiseasesSignal TransductionTransforming Growth Factor betaCalcineurinCalcineurin InhibitorsImmunosuppressive AgentsTransforming Growth Factor betacalcineurin inhibitorscalcineurin isoformsrenal fibrosis

Identifiers

PMID33225712
PMCPMC7988810
OpenAlexW3106978737

What OpenQuestion holds

Textmetadata
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.