Evidence map›Paper›PMID 35628326›Full record

ReviewInternational journal of molecular sciences2022

PAI-1: A Major Player in the Vascular Dysfunction in Obstructive Sleep Apnea?

Mohammad Badran, David Gozal

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 24 citations in OpenAlex.

  1. Trial
  2. SERPINE1 in ARDS: an emerging regulator of inflammation-coagulation-fibrinolysis crosstalk.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  3. Review
  4. Cardiovascular Toxicity of BTKi in Chronic B-Cell Malignancies.Reviews in cardiovascular medicine · 2026
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Genetic associations in sepsis and ARDS.Frontiers in pharmacology · 2026
    Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  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

2 authors at 1 institution in 1 country.

Mohammad BadranDepartment of Child Health and Child Health Research Institute, School of Medicine, University of Missouri, 400 N Keene St, Suite 010, Columbia, MO 65201, USA.ORCID 0000-0001-7073-741X
David GozalDepartment of Child Health and Child Health Research Institute, School of Medicine, University of Missouri, 400 N Keene St, Suite 010, Columbia, MO 65201, USA.ORCID 0000-0001-8195-6036
University of Missouri Health System · US

Funding

APP-mediated signaling, sleep perturbations, and Alzheimer's disease mouse modelsRF1AG061824 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI GOZAL, DAVID, PARENT, ANGELE · 2019 to 2019
$3.5M
NIA NIH HHS RF1 AG061824NIH HHS AG061824
6 · The paper itself

Abstract

Obstructive sleep apnea is a chronic and prevalent condition that is associated with endothelial dysfunction, atherosclerosis, and imposes excess overall cardiovascular risk and mortality. Despite its high prevalence and the susceptibility of CVD patients to OSA-mediated stressors, OSA is still under-recognized and untreated in cardiovascular practice. Moreover, conventional OSA treatments have yielded either controversial or disappointing results in terms of protection against CVD, prompting the need for the identification of additional mechanisms and associated adjuvant therapies. Plasminogen activator inhibitor-1 (PAI-1), the primary inhibitor of tissue-type plasminogen activator (tPA) and urinary-type plasminogen activator (uPA), is a key regulator of fibrinolysis and cell migration. Indeed, elevated PAI-1 expression is associated with major cardiovascular adverse events that have been attributed to its antifibrinolytic activity. However, extensive evidence indicates that PAI-1 can induce endothelial dysfunction and atherosclerosis through complex interactions within the vasculature in an antifibrinolytic-independent matter. Elevated PAI-1 levels have been reported in OSA patients. However, the impact of PAI-1 on OSA-induced CVD has not been addressed to date. Here, we provide a comprehensive review on the mechanisms by which OSA and its most detrimental perturbation, intermittent hypoxia (IH), can enhance the transcription of PAI-1. We also propose causal pathways by which PAI-1 can promote atherosclerosis in OSA, thereby identifying PAI-1 as a potential therapeutic target in OSA-induced CVD.

Indexed as

Antifibrinolytic AgentsAtherosclerosisCardiovascular SystemSleep Apnea, ObstructiveHumansPlasminogen Activator Inhibitor 1Antifibrinolytic AgentsPlasminogen Activator Inhibitor 1atherosclerosisendothelial dysfunctionintermittent hypoxiaobstructive sleep apneaplasminogen activator inhibitor-1

Identifiers

PMID35628326
PMCPMC9141273
OpenAlexW4280589337

What Socratic 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 Socratic graph.