ReviewJournal of molecular endocrinology2022
Going viral in the islet: mediators of SARS-CoV-2 entry beyond ACE2.
Review in Journal of molecular endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled 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.
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
14 citing papers in PubMed, 2 syntheses or guidelines pooled it, 18 citations in OpenAlex.
- Prevalence of new-onset diabetes following COVID-19 infection: A systematic review and meta-analysis.Diabetes, obesity & metabolism · 2026Pooled it
- Fetoplacental transmission and placental response to SARS-CoV-2: Evidence from the literature.Frontiers in medicine · 2022Pooled it
- Cadherin 1 negatively regulates SARS-CoV-2 infection in the olfactory epithelium.EMBO reports · 2026Article
- The silent epidemic within the pandemic: pathophysiology and prediction of post-COVID-19 diabetes.Journal of translational medicine · 2026Review
- Association of SARS-CoV-2 infection with incident diabetes among U.S. Veterans in a prospective longitudinal cohort.PloS one · 2026Article
- Vaccination and COVID-19: impact on long-COVID.Frontiers in immunology · 2025Review
- Potential Effects of Hyperglycemia on SARS-CoV-2 Entry Mechanisms in Pancreatic Beta Cells.Viruses · 2024Review
- Article
- New Insights into the Effects of SARS-CoV-2 on Metabolic Organs: A Narrative Review of COVID-19 Induced Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Diabetic Ketoacidosis and Long-term Insulin Requirements in Youths with Newly Diagnosed Type 2 Diabetes During the SARS-CoV-2 Pandemic.Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2023Article
- SARS-CoV-2 infection and its effects on the endocrine system.Best practice & research. Clinical endocrinology & metabolism · 2023Review
- Potential therapeutic applications of extracellular vesicles in the immunopathogenesis of COVID-19.Pathology, research and practice · 2023Review
- Antiviral Potential of Small Molecules Cordycepin, Thymoquinone, and N6, N6-Dimethyladenosine Targeting SARS-CoV-2 Entry Protein ADAM17.Molecules (Basel, Switzerland) · 2022Article
- Does diabetes risk after SARS-CoV-2 infection depend on the viral variant?Diabetes research and clinical practice · 2022Article
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
Abstract
Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Following initial infection of airway epithelia, SARS-CoV-2 invades a wide range of cells in multiple organs, including pancreatic islet cells. Diabetes is now recognised as a risk factor for severe COVID-19 outcomes, including hospitalisation and death. Additionally, COVID-19 is associated with a higher risk of new-onset diabetes and metabolic complications of diabetes. One mechanism by which these deleterious outcomes may occur is via the destruction of insulin-producing islet β cells, either directly by SARS-CoV-2 entry into β cells or indirectly due to inflammation and fibrosis in the surrounding microenvironment. While the canonical pathway of viral entry via angiotensin-converting enzyme 2 (ACE2) has been established as a major route of SARS-CoV-2 infection in the lung, it may not be solely responsible for viral entry into the endocrine pancreas. This is likely due to the divergent expression of viral entry factors among different tissues. For example, expression of ACE2 has not been unequivocally demonstrated in β cells. Thus, it is important to understand how other proteins known to be highly expressed in pancreatic endocrine cells may be involved in SARS-CoV-2 entry, with the view that these could be targeted to prevent the demise of the β cell in COVID-19. To that end, this review discusses alternate receptors of SARS-CoV-2 (CD147 and GRP78), as well as mediators (furin, TMPRSS2, cathepsin L, ADAM17, neuropilin-1, and heparan sulphate) that may facilitate SARS-CoV-2 entry into pancreatic islets independent of or in conjunction with ACE2.
Indexed as
Identifiers
What Socratic 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 Socratic graph.