Evidence map›Paper›PMID 38519981›Full record

ArticleCell communication and signaling : CCS2024

Inhibition of the MALT1-LPCAT3 axis protects cartilage degeneration and osteoarthritis.

Vijay Kondreddy, Rajkumar Banerjee, B L A Prabhavathi Devi, Kathirvel Muralidharan, Selvakumar Piramanayagam

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

Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
6.1field-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

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
  6. LPCAT3-dependent remodeling of the phospholipids and lipid rafts is essential for vascular proinflammatory signaling and the development of atherosclerosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  7. Review
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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 1 institution in 1 country.

Vijay KondreddyDepartment of Lipid Science and Technology, The Indian Institute of Chemical Technology, Uppal Road, Tarnaka, Hyderabad, 500007, India. vijay.667@csiriict.in.
Rajkumar BanerjeeDepartment of Lipid Science and Technology, The Indian Institute of Chemical Technology, Uppal Road, Tarnaka, Hyderabad, 500007, India.
B L A Prabhavathi DeviDepartment of Lipid Science and Technology, The Indian Institute of Chemical Technology, Uppal Road, Tarnaka, Hyderabad, 500007, India.
Kathirvel MuralidharanDivision of Applied Biology, The Indian Institute of Chemical Technology, Tarnaka, Hyderabad, India.
Selvakumar PiramanayagamDivision of Applied Biology, The Indian Institute of Chemical Technology, Tarnaka, Hyderabad, India.
Indian Institute of Chemical Technology · IN

Funding

Department of Science and Technology, Ministry of Science and Technology, India RJF/2021/000137
6 · The paper itself

Abstract

The proinflammatory cytokines and arachidonic acid (AA)-derived eicosanoids play a key role in cartilage degeneration in osteoarthritis (OA). The lysophosphatidylcholine acyltransferase 3 (LPCAT3) preferentially incorporates AA into the membranes. Our recent studies showed that MALT1 [mucosa-associated lymphoid tissue lymphoma translocation protein 1]) plays a crucial role in propagating inflammatory signaling triggered by IL-1β and other inflammatory mediators in endothelial cells. The present study shows that LPCAT3 expression was up-regulated in both human and mice articular cartilage of OA, and correlated with severity of OA. The IL-1β-induces cell death via upregulation of LPCAT3, MMP3, ADAMTS5, and eicosanoids via MALT1. Gene silencing or pharmacological inhibition of LPCAT3 or MALT1 in chondrocytes and human cartilage explants notably suppressed the IL-1β-induced cartilage catabolism through inhibition of expression of MMP3, ADAMTS5, and also secretion of cytokines and eicosanoids. Mechanistically, overexpression of MALT1 in chondrocytes significantly upregulated the expression of LPCAT3 along with MMP3 and ADAMTS5 via c-Myc. Inhibition of c-Myc suppressed the IL-1β-MALT1-dependent upregulation of LPCAT3, MMP3 and ADAMTS5. Consistent with the in vitro data, pharmacological inhibition of MALT1 or gene silencing of LPCAT3 using siRNA-lipid nanoparticles suppressed the synovial articular cartilage erosion, pro-inflammatory cytokines, and eicosanoids such as PGE

Indexed as

Cartilage, ArticularOsteoarthritis1-Acylglycerophosphocholine O-AcyltransferaseAnimalsCells, CulturedChondrocytesCytokinesEicosanoidsEndothelial CellsHumansInterleukin-1betaMatrix Metalloproteinase 3MiceMucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinRNA, Small Interfering1-Acylglycerophosphocholine O-AcyltransferaseCytokinesEicosanoidsInterleukin-1betaLPCAT3 protein, humanLPCAT3 protein, mouseMALT1 protein, humanMalt1 protein, mouseMatrix Metalloproteinase 3Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinRNA, Small InterferingCytokinesEicosanoidsLipid nanoparticlesLPCAT3MALT1Osteoarthritis

Identifiers

PMID38519981
PMCPMC10960471
OpenAlexW4393094556

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.