ArticleFrontiers in cellular neuroscience2021
Endothelial Senescence and Chronic Fatigue Syndrome, a COVID-19 Based Hypothesis.
Article in Frontiers in cellular neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis 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
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Biomarkers of post-acute infection syndrome: a systematic literature review.Frontiers in immunology · 2026Pooled it
- Trial
- Cardiovascular ageing: hallmarks, signaling pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Virus-induced endothelial senescence as a cause and driving factor for ME/CFS and long COVID: mediated by a dysfunctional immune system.Cell death & disease · 2026Review
- Main Dietary Patterns for Healthy Aging and Well-Being.Nutrients · 2025Review
- Core features and inherent diversity of post-acute infection syndromes.Frontiers in immunology · 2025Review
- Data-independent LC-MS/MS analysis of ME/CFS plasma reveals a dysregulated coagulation system, endothelial dysfunction, downregulation of complement machinery.Cardiovascular diabetology · 2024Article
- Association of circulating biomarkers with illness severity measures differentiates myalgic encephalomyelitis/chronic fatigue syndrome and post-COVID-19 condition: a prospective pilot cohort study.Journal of translational medicine · 2024Article
- Review
- Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: the biology of a neglected disease.Frontiers in immunology · 2024Review
- Vascular Ageing: Mechanisms, Risk Factors, and Treatment Strategies.International journal of molecular sciences · 2023Review
- COVID-19 and cellular senescence.Nature reviews. Immunology · 2023Review
- ME/CFS and Long COVID share similar symptoms and biological abnormalities: road map to the literature.Frontiers in medicine · 2023Review
- Neutrophil extracellular traps and long COVID.Frontiers in immunology · 2023Review
- The Gut Microbiome of Children during the COVID-19 Pandemic.Microorganisms · 2022Review
- Analysis of post COVID-19 condition and its overlap with myalgic encephalomyelitis/chronic fatigue syndrome.Journal of advanced research · 2022Review
- Perspective: Drawing on Findings From Critical Illness to Explain Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.Frontiers in medicine · 2022Article
- Article
- Virus-Induced Membrane Fusion in Neurodegenerative Disorders.Frontiers in cellular and infection microbiology · 2022Review
- The Infectious Bronchitis Coronavirus Pneumonia Model Presenting a Novel Insight for the SARS-CoV-2 Dissemination Route.Veterinary sciences · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
Abstract
Myalgic encephalomyelitis/chronic fatigue syndrome is a serious illness of unknown etiology, characterized by debilitating exhaustion, memory impairment, pain and sleep abnormalities. Viral infections are believed to initiate the pathogenesis of this syndrome although the definite proof remains elusive. With the unfolding of COVID-19 pandemic, the interest in this condition has resurfaced as excessive tiredness, a major complaint of patients infected with the SARS-CoV-2 virus, often lingers for a long time, resulting in disability, and poor life quality. In a previous article, we hypothesized that COVID-19-upregulated angiotensin II triggered premature endothelial cell senescence, disrupting the intestinal and blood brain barriers. Here, we hypothesize further that post-viral sequelae, including myalgic encephalomyelitis/chronic fatigue syndrome, are promoted by the gut microbes or toxin translocation from the gastrointestinal tract into other tissues, including the brain. This model is supported by the SARS-CoV-2 interaction with host proteins and bacterial lipopolysaccharide. Conversely, targeting microbial translocation and cellular senescence may ameliorate the symptoms of this disabling illness.
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.