Evidence map›Paper›PMID 37339050›Full record

ReviewCell reports2023

Reelin through the years: From brain development to inflammation.

Anna Alexander, Joachim Herz, Laurent Calvier

Open access · goldAbstract readReview
In one paragraph

Review in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
13.4field-weighted citation impact, top 1% 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

51 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
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  13. Neuroinflammation and Disease: Pathways and Opportunities.Annual review of pharmacology and toxicology · 2026
    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

3 authors at 1 institution in 1 country.

Anna AlexanderDepartment of Molecular Genetics, University of Texas (UT) Southwestern Medical Center, Dallas, TX, USA; Center for Translational Neurodegeneration Research, UT Southwestern Medical Center, Dallas, TX, USA.
Joachim HerzDepartment of Molecular Genetics, University of Texas (UT) Southwestern Medical Center, Dallas, TX, USA; Center for Translational Neurodegeneration Research, UT Southwestern Medical Center, Dallas, TX, USA; Department of Neuroscience, UT Southwestern Medical Center, Dallas, TX, USA; Department of Neurology and Neurotherapeutics, UT Southwestern Medical Center, Dallas, TX, USA.
Laurent CalvierDepartment of Molecular Genetics, University of Texas (UT) Southwestern Medical Center, Dallas, TX, USA; Center for Translational Neurodegeneration Research, UT Southwestern Medical Center, Dallas, TX, USA. Electronic address: calvier.laurent@gmail.com.
Southwestern Medical Center · US

Funding

UT Southwestern NORCP30DK127984 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI Jeffrey M Zigman · 2022 to 2026
$7.4M
Metabolism of the VLDL receptor and ApoE receptor 2R37HL063762 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HERZ, JOACHIM J · 2010 to 2019
$4.0M
METABOLISM OF THE VLDL RECEPTOR AND APOE RECEPTOR 2R01HL063762 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HERZ, JOACHIM J · 2000 to 2009
$3.1M
Physiology and Pathophysiology of Apolipoprotein E receptor-2 splicing in Alzheimer's diseaseRF1AG053391 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI HERZ, JOACHIM J · 2016 to 2020
$2.4M
Molecular Basis of Synaptic Suppression by ApoER01NS093382 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI HERZ, JOACHIM J · 2016 to 2020
$2.0M
NHLBI NIH HHS R01 HL063762NHLBI NIH HHS R37 HL063762NIA NIH HHS RF1 AG053391NIDDK NIH HHS P30 DK127984NINDS NIH HHS R01 NS093382
6 · The paper itself

Abstract

Reelin was originally identified as a regulator of neuronal migration and synaptic function, but its non-neuronal functions have received far less attention. Reelin participates in organ development and physiological functions in various tissues, but it is also dysregulated in some diseases. In the cardiovascular system, Reelin is abundant in the blood, where it contributes to platelet adhesion and coagulation, as well as vascular adhesion and permeability of leukocytes. It is a pro-inflammatory and pro-thrombotic factor with important implications for autoinflammatory and autoimmune diseases such as multiple sclerosis, Alzheimer's disease, arthritis, atherosclerosis, or cancer. Mechanistically, Reelin is a large secreted glycoprotein that binds to several membrane receptors, including ApoER2, VLDLR, integrins, and ephrins. Reelin signaling depends on the cell type but mostly involves phosphorylation of NF-κB, PI3K, AKT, or JAK/STAT. This review focuses on non-neuronal functions and the therapeutic potential of Reelin, while highlighting secretion, signaling, and functional similarities between cell types.

Indexed as

Cell Adhesion Molecules, NeuronalExtracellular Matrix ProteinsReelin ProteinBrainHumansInflammationLDL-Receptor Related ProteinsNerve Tissue ProteinsReceptors, LDLSerine EndopeptidasesCell Adhesion Molecules, NeuronalExtracellular Matrix ProteinsLDL-Receptor Related ProteinsNerve Tissue ProteinsReceptors, LDLReelin ProteinSerine EndopeptidasesAlzheimer’s diseaseApoER2arthritisatherosclerosiscancercoagulationCP: CancerCP: Immunologyimmune systeminflammationintestineJAK/STATkidneyleukocyteliverlymphatic circulationmultiple sclerosisNF-κBPI3K/AKTReelinvascular systemVLDR

Identifiers

PMID37339050
PMCPMC10592530
OpenAlexW4381249719

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.