Evidence map›Paper›PMID 41236634›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2025

LPCAT3-dependent remodeling of the phospholipids and lipid rafts is essential for vascular proinflammatory signaling and the development of atherosclerosis.

Vijay Kondreddy, Jhansi Magisetty, Pranshuta Rawat, Muralidharan Kathirvel, Ramchandra Reddy Jala, B L A Prabhavathi Devi, Sunil K Singh

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Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

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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

5 citing papers in PubMed.

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4 · The record

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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

7 authors.

Vijay KondreddyDepartment of Biochemistry, Central University of Punjab, Bathinda, 151401, India. kvijay.reddy@cup.edu.in.
Jhansi MagisettyDepartment of Zoology, Central University of Punjab, Bathinda, 151401, India. jhansi.lakshmi@cup.edu.in.
Pranshuta RawatDepartment of Zoology, Central University of Punjab, Bathinda, 151401, India.
Muralidharan KathirvelDivision of Applied Biology, The Indian Institute of Chemical Technology, Tarnaka, Hyderabad, India.
Ramchandra Reddy JalaDepartment of Oils, Lipid Science and Technology, Indian Institute of Chemical Technology, Hyderabad, India.
B L A Prabhavathi DeviDepartment of Oils, Lipid Science and Technology, Indian Institute of Chemical Technology, Hyderabad, India.
Sunil K SinghDepartment of Biochemistry, Central University of Punjab, Bathinda, 151401, India.

Funding

ANRF , India RJF/000137/2021ANRF, New Delhi, India ANRF/ECRG/2024/000820/LSDepartment of Health Research, Ministry of Health & Family Welfare, India SUG 2024-1136 reg
6 · The paper itself

Abstract

backgroundLysophosphatidyl choline acyltransferase 3 (LPCAT3) is crucially involved in the remodeling of phospholipids in the membranes through incorporation of arachidonic acid (ARA; 20:4). The ARA-derived eicosanoids aggravate leukocyte adhesion, inflammation, vascular dysfunction, thrombosis, and atherogenesis. This study found that LPCAT3 modulates lipid rafts and contributes to the raft assembly/organization essential for cytokine signaling.

methodsRNAi-dependent silencing of LPCAT3 in the endothelial cells. EPA and DHA enrichment in the cells. Lipid raft isolation and analysis of proinflammatory signaling molecules. Diet-induced atherosclerosis in the mice. LPCAT3 siRNA lipid nanoparticles/ EPA, DHA therapy.

resultsRNAi-dependent silencing of LPCAT3 inhibits TNFα-induced translocation & ubiquitination of TNFR1-signaling complex into the lipid rafts. This is associated with the attenuated NF-κB activation, synthesis of cell-adhesion molecules, cytokines, leukocyte adhesion, vascular permeability and endothelial dysfunction. Intriguingly, LPCAT3 inhibition resulted in significantly greater accretion of EPA and DHA in the PC and PE at the expense of ARA, and potentially decreased the ARA-derived eicosanoids in the vascular endothelium. Therapeutic administration of LPCAT3 siRNA-lipid nanoparticles in the high fat fed- mice markedly lowered the plasma glucose, insulin, proinflammatory cytokines, eicosanoids, and attenuated the plaque formation in the aorta. Co-treatment of LPCAT3 siRNA-lipid nanoparticles with EPA/DHA significantly elevated the accretion of EPA/DHA levels in the heart tissues and nullified the plaque development in the mice.

conclusionsOur data revealed that LPCAT3-dependent remodeling of lipid rafts is essential for the TNF-induced signal transduction, NF-kB activation, and vascular inflammation. Administration of LPCAT3 siRNA-lipid nanoparticles and EPA/DHA is an effective strategy to combat atherosclerosis.

Indexed as

1-Acylglycerophosphocholine O-AcyltransferaseAtherosclerosisMembrane MicrodomainsPhospholipidsAnimalsCytokinesDocosahexaenoic AcidsEicosapentaenoic AcidEndothelial CellsHumansMaleMiceMice, Inbred C57BLNanoparticlesNF-kappa BRNA, Small Interfering1-Acylglycerophosphocholine O-AcyltransferaseCytokinesDocosahexaenoic AcidsEicosapentaenoic AcidLPCAT3 protein, mouseNF-kappa BPhospholipidsRNA, Small InterferingTumor Necrosis Factor-alphaArachidonic acidEndotheliumFatty acidsInflammationLPCAT3Metabolism

Identifiers

PMID41236634

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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.