ReviewBioEssays : news and reviews in molecular, cellular and developmental biology2016
Missing heritability of complex diseases: Enlightenment by genetic variants from intermediate phenotypes.
Review in BioEssays : news and reviews in molecular, cellular and developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
What it found
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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
38 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Eleven genomic loci affect plasma levels of chronic inflammation marker soluble urokinase-type plasminogen activator receptor.Communications biology · 2021Pooled it
- Paternal SARS-CoV-2 infection impacts sperm small noncoding RNAs and increases anxiety in offspring in a sex-dependent manner.Nature communications · 2025Article
- Incorporating familial risk, lifestyle factors, and pharmacogenomic insights into personalized noncommunicable disease (NCD) reports for healthcare funder beneficiaries participating in the Open Genome Project.Annals of human genetics · 2025Article
- Multi-omics approaches for understanding gene-environment interactions in noncommunicable diseases: techniques, translation, and equity issues.Human genomics · 2025Review
- A Phenome-Wide Mendelian Randomization and Colocalization Study Reveals Genetic Association Between PBC and Other Autoimmune Disorders.Canadian journal of gastroenterology & hepatology · 2025Article
- Scrutinizing neurodegenerative diseases: decoding the complex genetic architectures through a multi-omics lens.Human genomics · 2024Review
- Endophenotype 2.0: updated definitions and criteria for endophenotypes of psychiatric disorders, incorporating new technologies and findings.Translational psychiatry · 2024Review
- Genetic risk score for coronary artery calcification and its predictive ability for coronary artery disease.American journal of preventive cardiology · 2024Article
- Computing linkage disequilibrium aware genome embeddings using autoencoders.Bioinformatics (Oxford, England) · 2024Article
- Identification of Genomic Regions Implicated in Susceptibility toInternational journal of molecular sciences · 2023Article
- Intermediate Molecular Phenotypes to Identify Genetic Markers of Anthracycline-Induced Cardiotoxicity Risk.Cells · 2023Article
- Identification of putative regulatory single-nucleotide variants in NTN1 gene associated with NSCL/P.Journal of human genetics · 2023Article
- A tractable physical model for the yeast polarity predicts epistasis and fitness.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Article
- Intermediate molecular phenotypes to identify genetic markers of anthracycline-induced cardiotoxicity risk.bioRxiv : the preprint server for biology · 2023Article
- Article
- Evolutionary Origins of Metabolic Reprogramming in Cancer.International journal of molecular sciences · 2022Review
- Transgenerational epigenetic impacts of parental infection on offspring health and disease susceptibility.Trends in genetics : TIG · 2022Review
- Integrative PheWAS analysis in risk categorization of major depressive disorder and identifying their associations with genetic variants using a latent topic model approach.Translational psychiatry · 2022Article
- L1 Retrotransposons: A Potential Endogenous Regulator for Schizophrenia.Frontiers in genetics · 2022Review
- Influence of the Human Lipidome on Epicardial Fat Volume in Mexican American Individuals.Frontiers in cardiovascular medicine · 2022Article
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7 authors.
Funding
Abstract
Diseases of complex origin have a component of quantitative genetics that contributes to their susceptibility and phenotypic variability. However, after several studies, a major part of the genetic component of complex phenotypes has still not been found, a situation known as "missing heritability." Although there have been many hypotheses put forward to explain the reasons for the missing heritability, its definitive causes remain unknown. Complex diseases are caused by multiple intermediate phenotypes involved in their pathogenesis and, very often, each one of these intermediate phenotypes also has a component of quantitative inheritance. Here we propose that at least part of the missing heritability can be explained by the genetic component of intermediate phenotypes that is not detectable at the level of the main complex trait. At the same time, the identification of the genetic component of intermediate phenotypes provides an opportunity to identify part of the missing heritability of complex diseases.
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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.