ArticleClinical science (London, England : 1979)2022
Vascular dysfunction in COVID-19 patients: update on SARS-CoV-2 infection of endothelial cells and the role of long non-coding RNAs.
Article in Clinical science (London, England : 1979), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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.
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.
Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Microvascular Dysfunction and Redox Imbalance in Long COVID.Microcirculation (New York, N.Y. : 1994) · 2026Article
- Translational MicroRNA research in COVID-19: bridging in Silico prediction with clinical biomarker potential.Clinical and experimental medicine · 2026Article
- Impaired Cardiovascular Hemodynamics in Patients Hospitalized with COVID-19 Pneumonia.Journal of clinical medicine · 2025Article
- Macrovascular Function in People with HIV After Recent SARS-CoV-2 Infection.Journal of vascular diseases · 2025Article
- Cerebromicrovascular mechanisms contributing to long COVID: implications for neurocognitive health.GeroScience · 2025Review
- Post-pandemic insights on COVID-19 and premature ovarian insufficiency.Open life sciences · 2025Review
- COVID-19 Exacerbates Neurovascular Uncoupling and Contributes to Endothelial Dysfunction in Patients with Mild Cognitive Impairment.Biomolecules · 2024Article
- Phenotypic switch of vascular smooth muscle cells in COVID-19: Role of cholesterol, calcium, and phosphate.Journal of cellular physiology · 2024Review
- Targeting PDGF/PDGFR Signaling Pathway by microRNA, lncRNA, and circRNA for Therapy of Vascular Diseases: A Narrow Review.Biomolecules · 2024Review
- Mitochondrial dysfunction in long COVID: mechanisms, consequences, and potential therapeutic approaches.GeroScience · 2024Review
- SARS-CoV-2 Spike Protein S1 Exposure Increases Susceptibility to Angiotensin II-Induced Hypertension in Rats by Promoting Central Neuroinflammation and Oxidative Stress.Neurochemical research · 2023Article
- The vascular perspective on acute and chronic lung disease.The Journal of clinical investigation · 2023Review
- Serum Catestatin Level as a Stratification Assessment Tool in Non-Critical COVID-19 Patients.International journal of environmental research and public health · 2023Article
- Cardiovascular-related proteomic changes in ECFCs exposed to the serum of COVID-19 patients.International journal of biological sciences · 2023Article
- Serial echocardiographic evaluation of COVID-19 patients without prior history of structural heart disease: a 1-year follow-up CRACoV-HHS study.Frontiers in cardiovascular medicine · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although COVID-19 is primarily a respiratory disease, it may affect also the cardiovascular system. COVID-19 patients with cardiovascular disorder (CVD) develop a more severe disease course with a significantly higher mortality rate than non-CVD patients. A common denominator of CVD is the dysfunction of endothelial cells (ECs), increased vascular permeability, endothelial-to-mesenchymal transition, coagulation, and inflammation. It has been assumed that clinical complications in COVID-19 patients suffering from CVD are caused by SARS-CoV-2 infection of ECs through the angiotensin-converting enzyme 2 (ACE2) receptor and the cellular transmembrane protease serine 2 (TMPRSS2) and the consequent dysfunction of the infected vascular cells. Meanwhile, other factors associated with SARS-CoV-2 entry into the host cells have been described, including disintegrin and metalloproteinase domain-containing protein 17 (ADAM17), the C-type lectin CD209L or heparan sulfate proteoglycans (HSPG). Here, we discuss the current data about the putative entry of SARS-CoV-2 into endothelial and smooth muscle cells. Furthermore, we highlight the potential role of long non-coding RNAs (lncRNAs) affecting vascular permeability in CVD, a process that might exacerbate disease in COVID-19 patients.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.