ReviewCell communication and signaling : CCS2025
Phospholipase D: emerging therapeutic targets in signaling, metabolism, and immune-oncology.
Review in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Novel compound heterozygous variants in theFrontiers in cardiovascular medicine · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The phospholipase D (PLD) family, comprising six evolutionarily conserved isoforms (PLD1-6), serves as master regulators of lipid signaling, membrane dynamics, and cellular communication. Functional divergence driven by structural heterogeneity enables PLD-mediated control of signal transduction, metabolic homeostasis, and immune responses. Activated by stimuli like growth factors and hormones, PLD governs core signaling networks, including Wnt/β-catenin, protein kinase C (PKC), and mammalian target of rapamycin (mTOR) pathways while modulating glucose uptake and lipid metabolism. PLD isoforms coordinate adaptive and innate immunity through T/B cell activation, macrophage polarization, and cytokine regulation. Dysregulated PLD activity promotes metabolic syndrome, autoimmune diseases, and remodeling of the tumor immune microenvironment, positioning PLD as a therapeutic target. This review integrates isoform-specific mechanisms in signaling, metabolism, immunity and tumor microenvironment, and underscores the critical need for isoform-specific inhibitors to dissect pathological mechanisms and advance disease understanding. By deconvoluting PLD's pleiotropic roles across signaling axis, lipid-glucose crosstalk, and immune circuitry, this work delineates a roadmap for developing targeted combinatorial therapies that exploit PLD's spatial-temporal regulation of cellular homeostasis.
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Registered trials
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 Socratic graph.