ArticlePLoS genetics2022
Proteome-wide Mendelian randomization identifies causal links between blood proteins and severe COVID-19.
Article in PLoS genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Identifying factors contributing to increased susceptibility to COVID-19 risk: a systematic review of Mendelian randomization studies.International journal of epidemiology · 2022Pooled it
- Explainable AI multiomics analysis reveals shared and divergent host responses in COVID-19 and influenza.NPJ digital medicine · 2026Article
- Identification of reactive CpGs and RNA expression in early COVID-19 through cis-eQTM analysis reflecting disease severity and recovery.Communications biology · 2025Article
- Exploring the impact of diet, sleep, and metabolomic pathways on Glaucoma subtypes: insights from Mendelian randomization and cross-sectional analyses.Nutrition & metabolism · 2025Article
- Evaluating metabolome-wide causal effects on risk for psychiatric and neurodegenerative disorders.BMC medicine · 2025Article
- Identification and validation of plasma protein biomarkers as therapeutic targets in acute myeloid leukemia: an integrative multi-omics study.Frontiers in immunology · 2025Article
- Proteome-Wide Mendelian Randomisation Identifies Causal Links of Plasma Proteins With Periodontitis.International dental journal · 2024Article
- Exploring Immune Cell Infiltration and Small Molecule Compounds for Ulcerative Colitis Treatment.Genes · 2024Article
- Circulating endocannabinoid levels in SARS-CoV-2 infection and their potential role in the inflammatory response.Scientific reports · 2024Article
- Article
- Article
- Article
- Proteomic Evolution from Acute to Post-COVID-19 Conditions.Journal of proteome research · 2024Article
- Plasma Proteome-Wide Mendelian Randomization Analysis Reveals Biomarkers and Therapeutic Targets for Different Stages of COVID-19.Transboundary and emerging diseases · 2024Article
- Development of a proteomic signature associated with severe disease for patients with COVID-19 using data from 5 multicenter, randomized, controlled, and prospective studies.Scientific reports · 2023Article
- Genetic Predisposition to Elevated Levels of Circulating ADAM17 Is Associated with the Risk of Severe COVID-19.International journal of molecular sciences · 2023Article
- Integrating plasma proteomes with genome-wide association data for causal protein identification in multiple myeloma.BMC medicine · 2023Article
- Genetic insight into the putative causal proteins and druggable targets of osteoporosis: a large-scale proteome-wide mendelian randomization study.Frontiers in genetics · 2023Article
- ABO blood group and link to COVID-19: A comprehensive review of the reported associations and their possible underlying mechanisms.Microbial pathogenesis · 2022Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 4 countries.
Funding
Abstract
In November 2021, the COVID-19 pandemic death toll surpassed five million individuals. We applied Mendelian randomization including >3,000 blood proteins as exposures to identify potential biomarkers that may indicate risk for hospitalization or need for respiratory support or death due to COVID-19, respectively. After multiple testing correction, using genetic instruments and under the assumptions of Mendelian Randomization, our results were consistent with higher blood levels of five proteins GCNT4, CD207, RAB14, C1GALT1C1, and ABO being causally associated with an increased risk of hospitalization or respiratory support/death due to COVID-19 (ORs = 1.12-1.35). Higher levels of FAAH2 were solely associated with an increased risk of hospitalization (OR = 1.19). On the contrary, higher levels of SELL, SELE, and PECAM-1 decrease risk of hospitalization or need for respiratory support/death (ORs = 0.80-0.91). Higher levels of LCTL, SFTPD, KEL, and ATP2A3 were solely associated with a decreased risk of hospitalization (ORs = 0.86-0.93), whilst higher levels of ICAM-1 were solely associated with a decreased risk of respiratory support/death of COVID-19 (OR = 0.84). Our findings implicate blood group markers and binding proteins in both hospitalization and need for respiratory support/death. They, additionally, suggest that higher levels of endocannabinoid enzymes may increase the risk of hospitalization. Our research replicates findings of blood markers previously associated with COVID-19 and prioritises additional blood markers for risk prediction of severe forms of COVID-19. Furthermore, we pinpoint druggable targets potentially implicated in disease pathology.
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.