Evidence map›Paper›PMID 34986238›Full record

ReviewBlood2022

Vasculopathy in COVID-19.

Robert Flaumenhaft, Keiichi Enjyoji, Alec A Schmaier

Open access · bronzeAbstract readReview
In one paragraph

Review in Blood, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
10.0field-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

74 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Cause of Death Analysis in a 9½-Year-Old with COVID-19 and Dravet Syndrome.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Article
  15. Article
  16. Article
  17. Coronary Implications of COVID-19.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2025
    Review
  18. Article
  19. Article
  20. Article

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

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

3 authors at 1 institution in 1 country.

Robert FlaumenhaftDivision  of Hemostasis and Thrombosis and.
Keiichi EnjyojiDivision  of Hemostasis and Thrombosis and.
Alec A SchmaierDivision  of Hemostasis and Thrombosis and.ORCID 0000-0002-4975-700X
Beth Israel Deaconess Medical Center · US

Funding

Thiol Isomerases in Hemostasis and ThrombosisR35HL135775 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI FLAUMENHAFT, ROBERT C · 2017 to 2023
$5.5M
Targeting the Endothelium in SepsisR01HL125275 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI FLAUMENHAFT, ROBERT C, PARIKH, SAMIR M · 2014 to 2018
$4.2M
Regulation of endothelial cell phosphatidylserine in thrombosisK08HL161259 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI Alec Andrew Schmaier · 2022 to 2026
$825k
NHLBI NIH HHS K08 HL161259NHLBI NIH HHS R01 HL125275NHLBI NIH HHS R35 HL135775
6 · The paper itself

Abstract

COVID-19 is a primary respiratory illness that is frequently complicated by systemic involvement of the vasculature. Vascular involvement leads to an array of complications ranging from thrombosis to pulmonary edema secondary to loss of barrier function. This review will address the vasculopathy of COVID-19 with a focus on the role of the endothelium in orchestrating the systemic response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. The endothelial receptor systems and molecular pathways activated in the setting of COVID-19 and the consequences of these inflammatory and prothrombotic changes on endothelial cell function will be discussed. The sequelae of COVID-19 vascular involvement at the level of organ systems will also be addressed, with an emphasis on the pulmonary vasculature but with consideration of effects on other vascular beds. The dramatic changes in endothelial phenotypes associated with COVID-19 has enabled the identification of biomarkers that could help guide therapy and predict outcomes. Knowledge of vascular pathogenesis in COVID-19 has also informed therapeutic approaches that may control its systemic sequelae. Because our understanding of vascular response in COVID-19 continues to evolve, we will consider areas of controversy, such as the extent to which SARS-CoV-2 directly infects endothelium and the degree to which vascular responses to SARS-CoV-2 are unique or common to those of other viruses capable of causing severe respiratory disease. This conceptual framework describing how SARS-CoV-2 infection affects endothelial inflammation, prothrombotic transformation, and barrier dysfunction will provide a context for interpreting new information as it arises addressing the vascular complications of COVID-19.

Indexed as

COVID-19ThrombosisVascular DiseasesHumansInflammationSARS-CoV-2

Identifiers

PMID34986238
PMCPMC8736280
OpenAlexW4206428633

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.