Evidence map›Paper›PMID 42421050›Full record

ArticleCell communication and signaling : CCS2026

Calcium signaling in human and mouse microglia exhibit differential susceptibility to phytocannabinoids.

Ivana Pilchova, Andrea Fleig, Reinhold Penner

Abstract read
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Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing 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

The trial behind it

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

Ivana PilchovaDepartment of Natural Sciences, Hawaii Pacific University, 900 Fort Street Mall, Suite 600, Honolulu, HI, 96813, USA. ivana.pilchova@uniba.sk.
Andrea FleigThe Queen's Center for Biomedical Research, The Queen's Medical Center, 1301 Punchbowl St, Honolulu, HI, 96813, USA.
Reinhold PennerDepartment of Natural Sciences, Hawaii Pacific University, 900 Fort Street Mall, Suite 600, Honolulu, HI, 96813, USA. rpenner@hawaii.edu.

Funding

Modulation of pain mechanisms by cannabis-derived phytochemicals.R01AT011162 · NCCIH · QUEEN'S MEDICAL CENTER · PI MACKIE, KENNETH, PENNER, REINHOLD · 2021 to 2025
$3.2M
NCCIH NIH HHS R01AT011162
6 · The paper itself

Abstract

backgroundNeurological disorders affect over 40% of the global population and are driven in part by microglia-mediated neuroinflammation that depends on calcium (Ca²⁺) signaling. Cannabis-derived compounds (CBx) modulate microglial activation and cytokine release, however, the impact of understudied CBx on Ca

methodsHere, we systematically examined the effects of over 22 CBx on key microglial Ca

resultsWe found that microglial SOCE in both mouse and human cell line models were potently inhibited by the same three, minor, acidic CBx - CBGA, CBGVA, CBDVA. In BV2, at least seven CBx (CBD, CBG, CBDVA, CBDA, CBGA, CBDV, CBNM) inhibited LPS-induced proinflammatory secretion of nitric oxide (NO) and TNF-α. Despite the profound SOCE inhibition in HMC3, CBx failed to inhibit downstream proinflammatory cytokine release in TNF-α - or IL-1β-activated cells. We found major differences in Ca

conclusionsThese findings provide a comprehensive qualitative and quantitative assessment of how individual CBx influence main Ca

Indexed as

Calcium SignalingCannabinoidsMicrogliaAnimalsCalciumCell LineCytokinesHumansMiceNitric OxideCalciumCannabinoidsCytokinesNitric OxideCalcium signalingCannabinoidsMicrogliaNeuroinflammationPurinergic receptorsStore-operated calcium entry

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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.