Evidence map›Paper›PMID 37103631›Full record

ReviewAngiogenesis2024

Damage to endothelial barriers and its contribution to long COVID.

Xiaoming Wu, Mengqi Xiang, Haijiao Jing, Chengyue Wang, Valerie A Novakovic, Jialan Shi

Open access · bronzeAbstract readReview
In one paragraph

Review in Angiogenesis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 4 pooled it
18.1field-weighted citation impact, top 1% 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

63 citing papers in PubMed, 4 syntheses or guidelines pooled it, 88 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Profiles of Individuals With Long COVID Reporting Persistent Cognitive Complaints.Archives of clinical neuropsychology : the official journal of the National Academy of Neuropsychologists · 2025
    Trial
  6. Treatment with Sulodexide Downregulates Biomarkers for Endothelial Dysfunction in Convalescent COVID-19 Patients.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
    Trial
  7. Review
  8. Article
  9. Review
  10. Article
  11. Observational
  12. Impact of Gestational Maternal SARS-CoV-2 Infection on Neonatal Inflammatory Biomarkers.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

3 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Xiaoming WuDepartment of Hematology, The First Hospital, Harbin Medical University, 150001, Harbin, China.
Mengqi XiangDepartment of Hematology, The First Hospital, Harbin Medical University, 150001, Harbin, China.
Haijiao JingDepartment of Hematology, The First Hospital, Harbin Medical University, 150001, Harbin, China.
Chengyue WangDepartment of Hematology, The First Hospital, Harbin Medical University, 150001, Harbin, China.
Valerie A NovakovicDepartment of Research, VA Boston Healthcare System, Harvard Medical School, Boston, MA, USA.
Jialan ShiDepartment of Hematology, The First Hospital, Harbin Medical University, 150001, Harbin, China. jialan_shi@dfci.harvard.edu.ORCID 0000-0001-5642-5436
Harbin Medical University · CNHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The world continues to contend with COVID-19, fueled by the emergence of viral variants. At the same time, a subset of convalescent individuals continues to experience persistent and prolonged sequelae, known as long COVID. Clinical, autopsy, animal and in vitro studies all reveal endothelial injury in acute COVID-19 and convalescent patients. Endothelial dysfunction is now recognized as a central factor in COVID-19 progression and long COVID development. Different organs contain different types of endothelia, each with specific features, forming different endothelial barriers and executing different physiological functions. Endothelial injury results in contraction of cell margins (increased permeability), shedding of glycocalyx, extension of phosphatidylserine-rich filopods, and barrier damage. During acute SARS-CoV-2 infection, damaged endothelial cells promote diffuse microthrombi and destroy the endothelial (including blood-air, blood-brain, glomerular filtration and intestinal-blood) barriers, leading to multiple organ dysfunction. During the convalescence period, a subset of patients is unable to fully recover due to persistent endothelial dysfunction, contributing to long COVID. There is still an important knowledge gap between endothelial barrier damage in different organs and COVID-19 sequelae. In this article, we mainly focus on these endothelial barriers and their contribution to long COVID.

Indexed as

COVID-19Vascular DiseasesAnimalsEndothelial CellsHumansPost-Acute COVID-19 SyndromeSARS-CoV-2Antithrombotic therapyEndothelial barrierLong COVIDVaccination

Identifiers

PMID37103631
PMCPMC10134732
OpenAlexW4367174681

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.