Evidence map›Paper›PMID 35144490›Full record

ReviewHypertension (Dallas, Tex. : 1979)2022

Role of Extracellular Vesicles in the Pathogenesis of Vascular Damage.

Fabrizio Buffolo, Silvia Monticone, Giovanni Camussi, Elena Aikawa

Open access · bronzeAbstract readReview
In one paragraph

Review in Hypertension (Dallas, Tex. : 1979), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

56 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Article
  3. Kidney-heart crosstalk: the extracellular vesicles connection.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026
    Review
  4. Observational
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Aging-Driven Inter-Organ Crosstalk in Postmenopausal Osteoporosis: From Immunometabolic Drift to Multisystem Frailty.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  18. Article
  19. Article
  20. Stroke, infections, and New Mechanisms: a Narrative Review.Current neurology and neuroscience reports · 2025
    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

4 authors at 3 institutions in 4 countries.

Fabrizio BuffoloDivision of Internal Medicine and Hypertension Unit, Department of Medical Sciences (F.B., S.M.), University of Torino, Italy.ORCID 0000-0001-9363-0199
Silvia MonticoneDivision of Internal Medicine and Hypertension Unit, Department of Medical Sciences (F.B., S.M.), University of Torino, Italy.ORCID 0000-0002-7322-2005
Giovanni CamussiDepartment of Medical Sciences, Molecular Biotechnology Center (G.C.), University of Torino, Italy.
Elena AikawaCenter for Interdisciplinary Cardiovascular Sciences, Department of Cardiovascular Medicine (F.B, E.A.), Brigham and Women's Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0001-7835-2135
Brigham and Women's Hospital · USAzienda Ospedaliero Universitaria San Giovanni Battista · ITDepartment of Medical Sciences · TH

Funding

Improving Mitral Compensation In Ischemic RegurgitationR01HL141917 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI AIKAWA, ELENA, BISCHOFF, JOYCE E. · 2018 to 2021
$5.6M
Macrophage-derived microcalcificaitonsR01HL136431 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI AIKAWA, ELENA · 2017 to 2020
$2.7M
New driver of fibrosis and calcification in CAVDR01HL147095 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI AIKAWA, ELENA · 2019 to 2022
$2.4M
NHLBI NIH HHS R01 HL136431NHLBI NIH HHS R01 HL141917NHLBI NIH HHS R01 HL147095
6 · The paper itself

Abstract

Extracellular vesicles (EVs) are nanosized membrane-bound structures released by cells that are able to transfer nucleic acids, protein cargos, and metabolites to specific recipient cells, allowing cell-to-cell communications in an endocrine and paracrine manner. Endothelial, leukocyte, and platelet-derived EVs have emerged both as biomarkers and key effectors in the development and progression of different stages of vascular damage, from earliest alteration of endothelial function, to advanced atherosclerotic lesions and cardiovascular calcification. Under pathological conditions, circulating EVs promote endothelial dysfunction by impairing vasorelaxation and instigate vascular inflammation by increasing levels of adhesion molecules, reactive oxygen species, and proinflammatory cytokines. Platelets, endothelial cells, macrophages, and foam cells secrete EVs that regulate macrophage polarization and contribute to atherosclerotic plaque progression. Finally, under pathological stimuli, smooth muscle cells and macrophages secrete EVs that aggregate between collagen fibers and serve as nucleation sites for ectopic mineralization in the vessel wall, leading to formation of micro- and macrocalcification. In this review, we summarize the emerging evidence of the pathological role of EVs in vascular damage, highlighting the major findings from the most recent studies and discussing future perspectives in this research field.

Indexed as

AtherosclerosisExtracellular VesiclesCell CommunicationEndothelial CellsHumansMacrophagesatherosclerosisendothelial dysfunctionextracellular vesicle vascular inflammationhypertensionvascular calcification

Identifiers

PMID35144490
PMCPMC9010370
OpenAlexW4210985886

What OpenQuestion 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 OpenQuestion graph.