Evidence map›Paper›PMID 38674016›Full record

ArticleInternational journal of molecular sciences2024

The CaMK Family Differentially Promotes Necroptosis and Mouse Cardiac Graft Injury and Rejection.

Haitao Lu, Jifu Jiang, Jeffery Min, Xuyan Huang, Patrick McLeod, Weihua Liu, Aaron Haig, Lakshman Gunaratnam, Anthony M Jevnikar, Zhu-Xu Zhang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Review
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

10 authors at 2 institutions in 1 country.

Haitao LuMatthew Mailing Centre for Translational Transplantation Studies, London Health Sciences Centre, London, ON N6A 5A5, Canada.ORCID 0000-0002-2461-2007
Jifu JiangMatthew Mailing Centre for Translational Transplantation Studies, London Health Sciences Centre, London, ON N6A 5A5, Canada.
Jeffery MinMatthew Mailing Centre for Translational Transplantation Studies, London Health Sciences Centre, London, ON N6A 5A5, Canada.
Xuyan HuangMatthew Mailing Centre for Translational Transplantation Studies, London Health Sciences Centre, London, ON N6A 5A5, Canada.
Patrick McLeodMatthew Mailing Centre for Translational Transplantation Studies, London Health Sciences Centre, London, ON N6A 5A5, Canada.
Weihua LiuDepartment of Pathology, Western University, London, ON N6A 3K7, Canada.
Aaron HaigDepartment of Pathology, Western University, London, ON N6A 3K7, Canada.
Lakshman GunaratnamMatthew Mailing Centre for Translational Transplantation Studies, London Health Sciences Centre, London, ON N6A 5A5, Canada.ORCID 0000-0002-8845-1126
Anthony M JevnikarMatthew Mailing Centre for Translational Transplantation Studies, London Health Sciences Centre, London, ON N6A 5A5, Canada.
Zhu-Xu ZhangMatthew Mailing Centre for Translational Transplantation Studies, London Health Sciences Centre, London, ON N6A 5A5, Canada.ORCID 0000-0002-8335-3738
Western University · CALondon Health Sciences Centre · CA

Funding

CIHR FRN169045
6 · The paper itself

Abstract

Organ transplantation is associated with various forms of programmed cell death which can accelerate transplant injury and rejection. Targeting cell death in donor organs may represent a novel strategy for preventing allograft injury. We have previously demonstrated that necroptosis plays a key role in promoting transplant injury. Recently, we have found that mitochondria function is linked to necroptosis. However, it remains unknown how necroptosis signaling pathways regulate mitochondrial function during necroptosis. In this study, we investigated the receptor-interacting protein kinase 3 (RIPK3) mediated mitochondrial dysfunction and necroptosis. We demonstrate that the calmodulin-dependent protein kinase (CaMK) family members CaMK1, 2, and 4 form a complex with RIPK3 in mouse cardiac endothelial cells, to promote trans-phosphorylation during necroptosis. CaMK1 and 4 directly activated the dynamin-related protein-1 (Drp1), while CaMK2 indirectly activated Drp1 via the phosphoglycerate mutase 5 (PGAM5). The inhibition of CaMKs restored mitochondrial function and effectively prevented endothelial cell death. CaMKs inhibition inhibited activation of CaMKs and Drp1, and cell death and heart tissue injury (n = 6/group,

Indexed as

DynaminsGraft RejectionHeart TransplantationNecroptosisReceptor-Interacting Protein Serine-Threonine KinasesAnimalsCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Endothelial CellsMaleMiceMice, Inbred C57BLMitochondriaPhosphoprotein PhosphatasesPhosphorylationSignal TransductionCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Dnm1l protein, mouseDynaminsPGAM5 protein, mousePhosphoprotein PhosphatasesReceptor-Interacting Protein Serine-Threonine KinasesRipk3 protein, mouseCaMKDrp1heartnecroptosisPGAM5transplantation

Identifiers

PMID38674016
PMCPMC11050252
OpenAlexW4394877381

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.