Evidence map›Paper›PMID 25128168›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2014

Aging impairs smooth muscle-mediated regulation of aortic stiffness: a defect in shock absorption function?

Yuan Z Gao, Robert J Saphirstein, Rina Yamin, Bela Suki, Kathleen G Morgan

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

43 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Integrin αScientific reports · 2026
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  7. Cardiovascular aging: spotlight on mitochondria.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Extracellular Matrix in Aging Aorta.Frontiers in cell and developmental biology · 2022
    Review
  17. Review
  18. Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Yuan Z GaoDepartment of Biomedical Engineering, College of Engineering, Boston University, Boston, Massachusetts; and Department of Health Sciences, Sargent College, Boston University, Boston, Massachusetts.
Robert J SaphirsteinDepartment of Health Sciences, Sargent College, Boston University, Boston, Massachusetts.
Rina YaminDepartment of Health Sciences, Sargent College, Boston University, Boston, Massachusetts.
Bela SukiDepartment of Biomedical Engineering, College of Engineering, Boston University, Boston, Massachusetts; and.
Kathleen G MorganDepartment of Health Sciences, Sargent College, Boston University, Boston, Massachusetts kmorgan@bu.edu.
Boston University · US

Funding

Structure-Function of the CytoskeletonP01HL086655 · NHLBI · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI MORGAN, KATHLEEN G · 2007 to 2011
$8.8M
Regulatory roles of variable mechanical stimuli in cell functionR01HL098976 · NHLBI · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI SUKI, BELA · 2009 to 2013
$2.3M
NHLBI NIH HHS HL-098976NHLBI NIH HHS P01 HL-086655
6 · The paper itself

Abstract

Increased aortic stiffness is an early and independent biomarker of cardiovascular disease. Here we tested the hypothesis that vascular smooth muscle cells (VSMCs) contribute significantly to aortic stiffness and investigated the mechanisms involved. The relative contributions of VSMCs, focal adhesions (FAs), and matrix to stiffness in mouse aorta preparations at optimal length and with confirmed VSMC viability were separated by the use of small-molecule inhibitors and activators. Using biomechanical methods designed for minimal perturbation of cellular function, we directly quantified changes with aging in aortic material stiffness. An alpha adrenoceptor agonist, in the presence of N(G)-nitro-l-arginine methyl ester (l-NAME) to remove interference of endothelial nitric oxide, increases stiffness by 90-200% from baseline in both young and old mice. Interestingly, increases are robustly suppressed by the Src kinase inhibitor PP2 in young but not old mice. Phosphotyrosine screening revealed, with aging, a biochemical signature of markedly impaired agonist-induced FA remodeling previously associated with Src signaling. Protein expression measurement confirmed a decrease in Src expression with aging. Thus we report here an additive model for the in vitro biomechanical components of the mouse aortic wall in which 1) VSMCs are a surprisingly large component of aortic stiffness at physiological lengths and 2) regulation of the VSMC component through FA signaling and hence plasticity is impaired with aging, diminishing the aorta's normal shock absorption function in response to stressors.

Indexed as

AgingStress, MechanicalVascular StiffnessAdrenergic AgonistsAnimalsAortaEnzyme InhibitorsFocal AdhesionsHemodynamicsMaleMiceMice, Inbred C57BLMyocytes, Smooth MuscleNG-Nitroarginine Methyl EsterPhenylephrinePyrimidinesAdrenergic AgonistsAG 1879Enzyme InhibitorsNG-Nitroarginine Methyl EsterPhenylephrinePyrimidinessrc-Family Kinasesalpha agonistfocal adhesionphosphotyrosinesmooth muscleSrc

Identifiers

PMID25128168
PMCPMC4200340
OpenAlexW2081463266

What OpenQuestion 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 OpenQuestion graph.