Evidence map›Paper›PMID 37626735›Full record

ReviewBiomedicines2023

Role of Endothelium in Cardiovascular Sequelae of Long COVID.

Luca Santoro, Vincenzo Zaccone, Lorenzo Falsetti, Vittorio Ruggieri, Martina Danese, Chiara Miro, Angela Di Giorgio, Antonio Nesci, Alessia D'Alessandro, Gianluca Moroncini and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
7.0field-weighted citation impact, top 2% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

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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

11 authors at 4 institutions in 1 country.

Luca SantoroDepartment of Cardiovascular and Thoracic Sciences, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy.ORCID 0000-0003-3614-7314
Vincenzo ZacconeDepartment of Emergency Medicine, Internal and Sub-Intensive Medicine, Azienda Ospedaliero-Universitaria delle Marche, 60126 Ancona, Italy.ORCID 0000-0002-5285-859X
Lorenzo FalsettiClinica Medica, Department of Clinical and Molecular Sciences, Università Politecnica delle Marche, 60126 Ancona, Italy.ORCID 0000-0003-3411-2388
Vittorio RuggieriDepartment of Internal Medicine, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.
Martina DaneseDepartment of Internal Medicine, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.
Chiara MiroDepartment of Internal Medicine, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.
Angela Di GiorgioDepartment of Cardiovascular and Thoracic Sciences, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy.
Antonio NesciDepartment of Cardiovascular and Thoracic Sciences, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy.
Alessia D'AlessandroDepartment of Cardiovascular and Thoracic Sciences, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy.
Gianluca MoronciniClinica Medica, Department of Clinical and Molecular Sciences, Università Politecnica delle Marche, 60126 Ancona, Italy.
Angelo SantoliquidoDepartment of Cardiovascular and Thoracic Sciences, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy.
Agostino Gemelli University Polyclinic · ITUniversità Cattolica del Sacro Cuore · ITMarche Polytechnic University · ITAzienda Ospedaliero Universitaria Ospedali Riuniti · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The global action against coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2 infection, shed light on endothelial dysfunction. Although SARS-CoV-2 primarily affects the pulmonary system, multiple studies have documented pan-vascular involvement in COVID-19. The virus is able to penetrate the endothelial barrier, damaging it directly or indirectly and causing endotheliitis and multi-organ injury. Several mechanisms cooperate to development of endothelial dysfunction, including endothelial cell injury and pyroptosis, hyperinflammation and cytokine storm syndrome, oxidative stress and reduced nitric oxide bioavailability, glycocalyx disruption, hypercoagulability, and thrombosis. After acute-phase infection, some patients reported signs and symptoms of a systemic disorder known as long COVID, in which a broad range of cardiovascular (CV) disorders emerged. To date, the exact pathophysiology of long COVID remains unclear: in addition to the persistence of acute-phase infection mechanisms, specific pathways of CV damage have been postulated, such as persistent viral reservoirs in the heart or an autoimmune response to cardiac antigens through molecular mimicry. The aim of this review is to provide an overview of the main molecular patterns of enduring endothelial activation following SARS-CoV-2 infection and to offer the latest summary of CV complications in long COVID.

Indexed as

cardiovascular diseaseendotheliumlong COVIDpost-acute sequelae SARS-CoV-2 infection (PASC)post-COVID-19SARS-CoV-2 infection

Identifiers

PMID37626735
PMCPMC10452509
OpenAlexW4385696903

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.