Evidence mapPaperPMID 39178024Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2024

Integrating molecular and cellular components of endothelial shear stress mechanotransduction.

Gavin Power, Larissa Ferreira-Santos, Luis A Martinez-Lemus, Jaume Padilla

Abstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
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

23 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

4 authors.

Gavin PowerNextGen Precision Health, University of Missouri, Columbia, Missouri, United States.ORCID 0000-0001-6147-8647
Larissa Ferreira-SantosNextGen Precision Health, University of Missouri, Columbia, Missouri, United States.ORCID 0000-0001-5738-1623
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

American Heart Association (AHA) 23PRE1020897American Heart Association (AHA) 24EIA1248820HHS | National Institutes of Health (NIH) R01HL153264NHLBI NIH HHS R01 HL153264
6 · The paper itself

Abstract

The lining of blood vessels is constantly exposed to mechanical forces exerted by blood flow against the endothelium. Endothelial cells detect these tangential forces (i.e., shear stress), initiating a host of intracellular signaling cascades that regulate vascular physiology. Thus, vascular health is tethered to the endothelial cells' capacity to transduce shear stress. Indeed, the mechanotransduction of shear stress underlies a variety of cardiovascular benefits, including some of those associated with increased physical activity. However, endothelial mechanotransduction is impaired in aging and disease states such as obesity and type 2 diabetes, precipitating the development of vascular disease. Understanding endothelial mechanotransduction of shear stress, and the molecular and cellular mechanisms by which this process becomes defective, is critical for the identification and development of novel therapeutic targets against cardiovascular disease. In this review, we detail the primary mechanosensitive structures that have been implicated in detecting shear stress, including junctional proteins such as platelet endothelial cell adhesion molecule-1 (PECAM-1), the extracellular glycocalyx and its components, and ion channels such as piezo1. We delineate which molecules are truly mechanosensitive and which may simply be indispensable for the downstream transmission of force. Furthermore, we discuss how these mechanosensors interact with other cellular structures, such as the cytoskeleton and membrane lipid rafts, which are implicated in translating shear forces to biochemical signals. Based on findings to date, we also seek to integrate these cellular and molecular mechanisms with a view of deciphering endothelial mechanotransduction of shear stress, a tenet of vascular physiology.

Indexed as

Endothelial CellsMechanotransduction, CellularStress, MechanicalAnimalsEndothelium, VascularGlycocalyxHumansIon ChannelsIon Channelsblood flowcytoskeletonendotheliumglycocalyxmechanosensation

Identifiers

PMID39178024
PMCPMC11482243

What Socratic holds

Textmetadata
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.