Evidence map›Paper›PMID 30333818›Full record

ReviewFrontiers in immunology2018

Calcium/Calmodulin Kinase IV Controls the Function of Both T Cells and Kidney Resident Cells.

Andrew P Ferretti, Rhea Bhargava, Shani Dahan, Maria G Tsokos, George C Tsokos

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Targeting FcRn for immunomodulation: a promising therapy in autoimmune inflammatory rheumatic diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Impaired CAMK4 Activity Limits Atherosclerosis and Reprograms Myelopoiesis.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Article
  8. CaMK modulates sensory neural activity to control longevity and proteostasis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. New anti-cancer explorations based on metal ions.Journal of nanobiotechnology · 2022
    Review
  17. Article
  18. Review
  19. Article
  20. CaJournal of cellular immunology · 2021
    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

5 authors at 2 institutions in 1 country.

Andrew P FerrettiDepartment of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States.
Rhea BhargavaDepartment of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States.
Shani DahanDepartment of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States.
Maria G TsokosDepartment of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States.
George C TsokosDepartment of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States.
Harvard University · USBeth Israel Deaconess Medical Center · US

Funding

MOLECULAR BASIS OF ALLERGIC AND IMMUNOLOGIC DISEASET32AI007512 · NIAID · CHILDREN'S HOSPITAL BOSTON · PI Janet Chou, Peter A Nigrovic · 1996 to 2026
$13.1M
Targeting CaMK4 in SLER01AR064350 · NIAMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TSOKOS, GEORGE C · 2013 to 2017
$1.8M
NIAID NIH HHS T32 AI007512NIAMS NIH HHS R01 AR064350
6 · The paper itself

Abstract

Calcium calmodulin kinase IV (CaMK4) regulates multiple processes that significantly contribute to the lupus-related pathology by controlling the production of IL-2 and IL-17 by T cells, the proliferation of mesangial cells, and the function and structure of podocytes. CaMK4 is also upregulated in podocytes from patients with focal segmental glomerulosclerosis (FSGS). In both immune and non-immune podocytopathies, CaMK4 disrupts the structure and function of podocytes. In lupus-prone mice, targeted delivery of a CaMK4 inhibitor to CD4

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 4Glomerulosclerosis, Focal SegmentalHumansInterleukin-2Lupus NephritisMesangial CellsMiceMolecular Targeted TherapyPodocytesTh17 CellsT-Lymphocytes, RegulatoryCalcium-Calmodulin-Dependent Protein Kinase Type 4CAMK4 protein, humanCamk4 protein, mouseInterleukin-2calcium/calmodulin kinase IVCaMK4IL-17IL-2 deprivationpodocyte dysfunctionTreg deficiency

Identifiers

PMID30333818
PMCPMC6176098
OpenAlexW2894609084

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.