Article in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing 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.
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
13 authors.
Philipp JakobsCardiovascular Degeneration, Haendeler Group, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital and Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany.ORCID 0009-0007-9249-4042
Anne RafflenbeulCardiovascular Degeneration, Altschmied Group, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital and Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany.ORCID 0009-0002-2234-9038
Willem Berend PostInstitute of Cell Biology, Department of Biology, Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany.ORCID 0000-0002-2552-6477
Niloofar Ale-AghaCardiovascular Degeneration, Haendeler Group, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital and Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany.ORCID 0009-0003-7350-1367
Victoria Elisabeth GroßInstitute of Cell Biology, Department of Biology, Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany.ORCID 0000-0001-9131-490X
Stephanie PickInstitute of Cell Biology, Department of Biology, Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany.ORCID 0009-0005-1325-0812
Sascha DolataInstitute of Cell Biology, Department of Biology, Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany.
Fiona F CoxCardiovascular Degeneration, Altschmied Group, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital and Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany.
Florian von AmelnCardiovascular Degeneration, Altschmied Group, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital and Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany.
Olaf EckermannCardiovascular Degeneration, Haendeler Group, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital and Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany.
Joachim AltschmiedCardiovascular Degeneration, Altschmied Group, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital and Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany.ORCID 0000-0001-9617-9559
Simone PrömelInstitute of Cell Biology, Department of Biology, Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany.ORCID 0000-0001-7800-7323
Judith HaendelerCardiovascular Degeneration, Haendeler Group, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital and Heinrich Heine University Düsseldorf, 40225 Düsseldorf, Germany.ORCID 0000-0001-8507-4540
Funding
University of Düsseldorf, Medical Faculty 9792888
6 · The paper itself
Abstract
The most common trigger of sepsis and septic shock is bacterial lipopolysaccharide (LPS). Endothelial cells are among the first to encounter LPS directly. Generally, their function is closely linked to active endothelial NO Synthase (eNOS), which is significantly reduced under septic conditions. LPS treatment of endothelial cells leads to their activation and apoptosis, resulting in loss of integrity and vascular leakage, a hallmark of septic shock. Hence, therapies that prevent endothelial leakage or restore the endothelial barrier would be invaluable for patients. Adhesion GPCRs (aGPCRs) have been largely overlooked in this context, although particularly one of them, ADGRL2/LPHN2, has been implicated in endothelial barrier function. Our study shows that overexpression of ADGRL2 protects endothelial cells from LPS-induced activation, apoptosis, and impaired migration. Mechanistically, ADGRL2 preserves eNOS activity by shifting its binding from Caveolin-1 to Heat Shock Protein 90. Furthermore, ADGRL2 enhances antioxidative responses by increasing NRF2 activity. Notably, we found that this function may be evolutionarily conserved. In the absence of
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.
The Adhesion GPCR ADGRL2/LPHN2 Can Protect Against Cellular and Organismal Dysfunction. · full record | OpenQuestion