Evidence map›Paper›PMID 41872265›Full record

ArticleScientific reports2026

Voltage-gated calcium channels as key regulators of neuronal differentiation in the immortalized dorsal root ganglion neuronal cell line F11.

D López, J Brea, M Barro, M I Loza, A L Martínez

Abstract read
In one paragraph

Article in Scientific reports, 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
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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

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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

5 authors.

D LópezInnopharma Drug Screening and Pharmacogenomics Platform, BioFarma Research Group, Department of Pharmacology, Pharmacy and Pharmaceutical Technology, Center for Research in Molecular Medicine and Chronic Diseases (CiMUS), University of Santiago de Compostela and IDIS (Health Research Institute of Santiago de Compostela), Santiago de Compostela, Spain.
J BreaInnopharma Drug Screening and Pharmacogenomics Platform, BioFarma Research Group, Department of Pharmacology, Pharmacy and Pharmaceutical Technology, Center for Research in Molecular Medicine and Chronic Diseases (CiMUS), University of Santiago de Compostela and IDIS (Health Research Institute of Santiago de Compostela), Santiago de Compostela, Spain.
M BarroInnopharma Drug Screening and Pharmacogenomics Platform, BioFarma Research Group, Department of Pharmacology, Pharmacy and Pharmaceutical Technology, Center for Research in Molecular Medicine and Chronic Diseases (CiMUS), University of Santiago de Compostela and IDIS (Health Research Institute of Santiago de Compostela), Santiago de Compostela, Spain.
M I LozaInnopharma Drug Screening and Pharmacogenomics Platform, BioFarma Research Group, Department of Pharmacology, Pharmacy and Pharmaceutical Technology, Center for Research in Molecular Medicine and Chronic Diseases (CiMUS), University of Santiago de Compostela and IDIS (Health Research Institute of Santiago de Compostela), Santiago de Compostela, Spain. mabel.loza@usc.es.
A L MartínezInnopharma Drug Screening and Pharmacogenomics Platform, BioFarma Research Group, Department of Pharmacology, Pharmacy and Pharmaceutical Technology, Center for Research in Molecular Medicine and Chronic Diseases (CiMUS), University of Santiago de Compostela and IDIS (Health Research Institute of Santiago de Compostela), Santiago de Compostela, Spain. antonleandro.martinez@usc.es.

Funding

Agencia Estatal de Investigación PID2023-146870OB-I00Xunta de Galicia ED431C 2022/20
6 · The paper itself

Abstract

Calcium signaling is essential for neuronal development and function, yet its role in the differentiation of immortalized neuronal cell lines remains poorly understood. In this study, we investigated the involvement of voltage-gated calcium channels (VGCCs) in the differentiation of the F11 cell line, a widely used translational model derived from the fusion of mouse neuroblastoma cells with rat dorsal root ganglion neurons. Differentiation was associated with greater KCl-evoked increases in intracellular Ca2+ and with upregulated expression of VGCC-encoding genes, particularly those for L-type channels. Pharmacological inhibition of L-type VGCCs reduced the KCl-evoked intracellular Ca2+ increase and impaired neurite outgrowth, underscoring their role in differentiation. Additionally, overexpression of CaV1.3 in non-differentiated F11 cells enhanced neuronal features, including greater KCl-evoked increases in intracellular Ca2+ and neurite outgrowth. However, under differentiation conditions, CaV1.3 overexpression disrupted the acquisition of neuronal features and coincided with increased intracellular oxidative stress. Notably, this effect was more pronounced for CaV1.3 than for the higher activation-threshold CaV1.2 channels. These findings highlight the dual role of L-type VGCCs in neuronal differentiation and oxidative stress regulation, demonstrating that their precise modulation is critical for proper neuronal development. Moreover, the shared molecular pathways between F11 cell differentiation and neurogenesis reinforce the translational value of this model for drug discovery efforts targeting oxidative stress-mediated neuronal dysfunction, such as in neurodegenerative diseases and neuropathic pain.

Indexed as

Calcium Channels, L-TypeCell DifferentiationGanglia, SpinalNeuronsAnimalsCalciumCalcium SignalingCell LineMiceNeurogenesisOxidative StressPotassium ChlorideRatsCalciumCalcium Channels, L-TypePotassium Chloride

Identifiers

PMID41872265
PMCPMC13153280

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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.