Evidence mapPaperPMID 41544633Full record

ArticleAmerican journal of physiology. Cell physiology2026

ADAM17-induced shedding of glypican-1 as a mechanism of impaired endothelial shear stress mechanotransduction.

Marc A Augenreich, Larissa Ferreira-Santos, Gavin Power, Francisco I Ramirez-Perez, Juan D Gonzalez-Vallejo, Morgan B Williams, Natnicha Imkaew, Min Jeong Cho, Andrew A Wheeler, Camila Manrique-Acevedo and 2 more

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2026. 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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
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

12 authors.

Marc A AugenreichNextGen Precision Health, University of Missouri, Columbia, Missouri, United States.ORCID 0000-0002-0719-8799
Larissa Ferreira-SantosNextGen Precision Health, University of Missouri, Columbia, Missouri, United States.ORCID 0000-0001-5738-1623
Gavin PowerNextGen Precision Health, University of Missouri, Columbia, Missouri, United States.ORCID 0000-0001-6147-8647
Francisco I Ramirez-PerezNextGen Precision Health, University of Missouri, Columbia, Missouri, United States.ORCID 0000-0003-4920-383X
Juan D Gonzalez-VallejoNextGen Precision Health, University of Missouri, Columbia, Missouri, United States.ORCID 0000-0002-4682-6030
Morgan B WilliamsNextGen Precision Health, University of Missouri, Columbia, Missouri, United States.
Natnicha ImkaewNextGen Precision Health, University of Missouri, Columbia, Missouri, United States.ORCID 0009-0000-9675-2765
Min Jeong ChoNextGen Precision Health, University of Missouri, Columbia, Missouri, United States.ORCID 0000-0002-5562-4609
Andrew A WheelerDepartment of Surgery, University of Missouri, Columbia, Missouri, United States.ORCID 0000-0002-8675-887X
Camila Manrique-AcevedoNextGen Precision Health, University of Missouri, Columbia, Missouri, United States.ORCID 0000-0001-9341-404X
Luis A Martinez-LemusNextGen Precision Health, University of Missouri, Columbia, Missouri, United States.ORCID 0000-0002-6559-5717
Jaume PadillaNextGen Precision Health, University of Missouri, Columbia, Missouri, United States.ORCID 0000-0002-7944-4936

Funding

Targeting ADAM17 activity for correction of vascular insulin resistance in type 2 diabetesR01HL151384 · UNIVERSITY OF MISSOURI-COLUMBIA · 2025 to 2025
$682k
American Heart Association (AHA) 23PRE1020897American Heart Association (AHA) 24EIA1248820American Heart Association (AHA) 25DIVSUP1463861Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) 2024/09267-4HHS | National Institutes of Health (NIH) R01HL137769HHS | National Institutes of Health (NIH) R01HL151384HHS | National Institutes of Health (NIH) R01HL153264HHS | National Institutes of Health (NIH) R21DK116081NHLBI NIH HHS R01 HL137769NHLBI NIH HHS R01 HL151384NHLBI NIH HHS R01 HL153264NIDDK NIH HHS R21 DK116081
6 · The paper itself

Abstract

Endothelial dysfunction occurs early in the pathogenesis of type 2 diabetes (T2D)-associated cardiovascular disease. Previous work has revealed that endothelial glycocalyx mechanosensing structures are degraded in T2D, likely contributing to impaired shear stress mechanotransduction and consequent blunted vasodilation. Evidence from proteomic analysis suggests that glypican-1, a well-known mechanosensor, is a substrate of the proinflammatory enzyme ADAM17. A critical step in ADAM17 activation is externalization of phosphatidylserine (PS) to the outer leaflet of the plasmalemma, which can be enacted by the Ca

Indexed as

ADAM17 ProteinDiabetes Mellitus, Type 2Endothelial CellsEndothelium, VascularGlypicansMechanotransduction, CellularAnimalsAnoctaminsFemaleGlycocalyxHumansMaleMiceMice, Inbred C57BLMice, KnockoutNeuraminidaseADAM17 ProteinADAM17 protein, humanAdam17 protein, mouseANO6 protein, humanAnoctaminsGlypicansNeuraminidasePhospholipid Transfer ProteinsADAM17ANO6flow-mediated dilationglypican-1neuraminidase

Identifiers

PMID41544633
PMCPMC12905800

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.