Evidence map›Paper›PMID 34566697›Full record

ReviewFrontiers in physiology2021

The Mechanobiology of Endothelial-to-Mesenchymal Transition in Cardiovascular Disease.

Shahrin Islam, Kristina I Boström, Dino Di Carlo, Craig A Simmons, Yin Tintut, Yucheng Yao, Jeffrey J Hsu

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Subclinical Changes in Cardiovascular Function During the Neonatal Period in Infants Born to Mothers With Diabetes.The journal of pediatric pharmacology and therapeutics : JPPT : the official journal of PPAG · 2026
    Article
  7. Article
  8. TRPV4-Mediated Mechanosensing Regulates the Endothelial-to-Mesenchymal Transition: Implications for Atherosclerosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review
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

7 authors at 2 institutions in 2 countries.

Shahrin IslamDivision of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States.
Kristina I BoströmDivision of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States.
Dino Di CarloDepartment of Bioengineering, University of California, Los Angeles, Los Angeles, CA, United States.
Craig A SimmonsDepartment of Mechanical and Industrial Engineering, University of Toronto, Toronto, ON, Canada.
Yin TintutDivision of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States.
Yucheng YaoDivision of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States.
Jeffrey J HsuDivision of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States.
University of California, Los Angeles · USUniversity of Toronto · CA

Funding

Molecular Mechanisms of MGP; Role in AVMsR01HL081397 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BOSTROM, KRISTINA I · 2006 to 2025
$7.7M
BMP and Notch Crosstalk in Cerebral Arteriovenous MalformationsR01NS079353 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Yucheng Yao · 2012 to 2026
$5.3M
Switch of Osteogenesis in Vascular CalcificationR01HL139675 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Yucheng Yao · 2018 to 2026
$3.6M
Role of intermittent activation of parathyroid hormone receptor in exercise-induced vascular calcificationR01HL151391 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEMER, LINDA L., TINTUT, YIN · 2021 to 2024
$2.2M
Endothelial Regulation of Vascular CalcificationR01HL158053 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BOSTROM, KRISTINA I · 2022 to 2025
$2.2M
Serotonin receptor contribution to inflammation-induced calcific aortic valve diseaseR01HL137647 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEMER, LINDA L., TINTUT, YIN · 2019 to 2022
$1.6M
Mechanobiology of Endothelial-to-Mesenchymal Transition in Cardiovascular CalcificationK08HL151961 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HSU, JEFFREY JOHN · 2020 to 2024
$646k
NHLBI NIH HHS K08 HL151961NHLBI NIH HHS R01 HL081397NHLBI NIH HHS R01 HL137647NHLBI NIH HHS R01 HL139675NHLBI NIH HHS R01 HL151391NHLBI NIH HHS R01 HL158053NINDS NIH HHS R01 NS079353
6 · The paper itself

Abstract

Endothelial cells (ECs) lining the cardiovascular system are subjected to a highly dynamic microenvironment resulting from pulsatile pressure and circulating blood flow. Endothelial cells are remarkably sensitive to these forces, which are transduced to activate signaling pathways to maintain endothelial homeostasis and respond to changes in the environment. Aberrations in these biomechanical stresses, however, can trigger changes in endothelial cell phenotype and function. One process involved in this cellular plasticity is endothelial-to-mesenchymal transition (EndMT). As a result of EndMT, ECs lose cell-cell adhesion, alter their cytoskeletal organization, and gain increased migratory and invasive capabilities. EndMT has long been known to occur during cardiovascular development, but there is now a growing body of evidence also implicating it in many cardiovascular diseases (CVD), often associated with alterations in the cellular mechanical environment. In this review, we highlight the emerging role of shear stress, cyclic strain, matrix stiffness, and composition associated with EndMT in CVD. We first provide an overview of EndMT and context for how ECs sense, transduce, and respond to certain mechanical stimuli. We then describe the biomechanical features of EndMT and the role of mechanically driven EndMT in CVD. Finally, we indicate areas of open investigation to further elucidate the complexity of EndMT in the cardiovascular system. Understanding the mechanistic underpinnings of the mechanobiology of EndMT in CVD can provide insight into new opportunities for identification of novel diagnostic markers and therapeutic interventions.

Indexed as

biomechanicalcardiovascular diseaseendothelialendothelial-to-mesenchymal transitionmechanobiologymesenchymal

Identifiers

PMID34566697
PMCPMC8458763
OpenAlexW3197421733

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.