Evidence map›Paper›PMID 37398237›Full record

ArticlemedRxiv : the preprint server for health sciences2023

Abnormal lymphatic S1P signaling aggravates lymphatic dysfunction and tissue inflammation.

Dongeon Kim, Wen Tian, Timothy Ting-Hsuan Wu, Menglan Xiang, Ryan Vinh, Jason Chang, Shenbiao Gu, Seunghee Lee, Yu Zhu, Torrey Guan and 8 more

Open access · greenAbstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in medRxiv : the preprint server for health sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
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

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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 3 institutions in 1 country.

Dongeon KimVA Palo Alto Health Care System, Palo Alto, California, USA.
Wen TianVA Palo Alto Health Care System, Palo Alto, California, USA.
Timothy Ting-Hsuan WuStanford University School of Medicine, Stanford, California, USA.
Menglan XiangVA Palo Alto Health Care System, Palo Alto, California, USA.
Ryan VinhVA Palo Alto Health Care System, Palo Alto, California, USA.
Jason ChangVA Palo Alto Health Care System, Palo Alto, California, USA.
Shenbiao GuVA Palo Alto Health Care System, Palo Alto, California, USA.
Seunghee LeeVA Palo Alto Health Care System, Palo Alto, California, USA.
Yu ZhuVA Palo Alto Health Care System, Palo Alto, California, USA.
Torrey GuanVA Palo Alto Health Care System, Palo Alto, California, USA.
Emilie Claire SchneiderVA Palo Alto Health Care System, Palo Alto, California, USA.
Evan BaoVA Palo Alto Health Care System, Palo Alto, California, USA.
J Brandon DixonGeorgia Institute of Technology, Atlanta, Georgia, USA.
Peter KaoStanford University School of Medicine, Stanford, California, USA.
Junliang PanVA Palo Alto Health Care System, Palo Alto, California, USA.
Stanley G RocksonStanford University School of Medicine, Stanford, California, USA.
Xinguo JiangVA Palo Alto Health Care System, Palo Alto, California, USA.
Mark Robert NicollsVA Palo Alto Health Care System, Palo Alto, California, USA.
VA Palo Alto Health Care System · USStanford University · USGeorgia Institute of Technology · US

Funding

A Critical Role for Leukotriene B4 in LymphedemaR01HL141105 · NHLBI · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI NICOLLS, MARK ROBERT · 2019 to 2022
$2.3M
A Critical Role for Hypoxia-Inducible Factors in LymphedemaR01HL150583 · NHLBI · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI JIANG, XINGUO · 2021 to 2024
$2.3M
NHLBI NIH HHS R01 HL141105NHLBI NIH HHS R01 HL150583
6 · The paper itself

Abstract

backgroundLymphedema is a global health problem with no effective drug treatment. Enhanced T cell immunity and abnormal lymphatic endothelial cell (LEC) signaling are promising therapeutic targets for this condition. Sphingosine-1-phosphate (S1P) mediates a key signaling pathway required for normal LEC function, and altered S1P signaling in LECs could lead to lymphatic disease and pathogenic T cell activation. Characterizing this biology is relevant for developing much-needed therapies.

methodsHuman and mouse lymphedema was studied. Lymphedema was induced in mice by surgically ligating the tail lymphatics. Lymphedematous dermal tissue was assessed for S1P signaling. To verify the role of altered S1P signaling effects in lymphatic cells, LEC-specific

resultsHuman and experimental lymphedema tissues exhibited decreased LEC S1P signaling through S1PR1. LEC

conclusionThis study suggests that reduction of the LEC S1P signaling aggravates lymphedema by enhancing LEC adhesion and amplifying pathogenic CD4 T cell responses. P-selectin inhibitors are suggested as a possible treatment for this pervasive condition. Clinical Perspective:

Identifiers

PMID37398237
PMCPMC10312855
OpenAlexW4380361387

What OpenQuestion holds

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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.