ArticleKidney international2019
Uncovering genetic mechanisms of kidney aging through transcriptomics, genomics, and epigenomics.
Article in Kidney international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Discovery of rare variants associated with blood pressure regulation through meta-analysis of 1.3 million individuals.Nature genetics · 2020Pooled it
- Article
- Shorter kidney telomeres are associated with nephrosclerosis by an epigenetic signature.Cardiovascular research · 2026Article
- Kidney Disease as a Driver of Immunosenescence: Mechanisms and Potential Interventions.Journal of the American Society of Nephrology : JASN · 2026Review
- Gene Expression as a Guide for the Development of Novel Therapies in Hypertensive and Diabetic Kidney Disease.Journal of clinical medicine · 2026Article
- MRI-based multi-organ clocks for healthy aging and disease assessment.Nature medicine · 2026Article
- Integrative multi-omics profiling for early diagnosis, stratification and personalized management of chronic kidney disease: a new paradigm.Clinical and experimental medicine · 2025Review
- Transcript diversity in aging: cryptic transcription and splicing.Medical review (2021) · 2025Review
- Multi-organ MRI digitizes biological aging clocks across proteomics, metabolomics, and genetics.medRxiv : the preprint server for health sciences · 2025Article
- Article
- The boundaries of normal kidney tissue for biomedical research.Current opinion in nephrology and hypertension · 2025Review
- A multi-modal fusion model with enhanced feature representation for chronic kidney disease progression prediction.Briefings in bioinformatics · 2024Article
- Genetic imputation of kidney transcriptome, proteome and multi-omics illuminates new blood pressure and hypertension targets.Nature communications · 2024Article
- Insights into the Cellular Localization and Functional Properties of TSPYL5 Protein.International journal of molecular sciences · 2023Article
- Assessing Kidney Injury Induced by Mercuric Chloride in Guinea Pigs with In Vivo and In Vitro Experiments.International journal of molecular sciences · 2023Article
- DNA-dependent protein kinase catalytic subunit (DNA-PKcs) drives chronic kidney disease progression in male mice.Nature communications · 2023Article
- LTF induces senescence and degeneration in the meniscus via the NF-κB signaling pathway: A study based on integrated bioinformatics analysis and experimental validation.Frontiers in molecular biosciences · 2023Article
- Contributions of obesity to kidney health and disease: insights from Mendelian randomization and the human kidney transcriptomics.Cardiovascular research · 2022Article
- Kidney omics in hypertension: from statistical associations to biological mechanisms and clinical applications.Kidney international · 2022Review
- Review
Corrections and comments
- Commented on by
Authors and funding
20 authors at 10 institutions in 3 countries.
Funding
Abstract
Nephrons scar and involute during aging, increasing the risk of chronic kidney disease. Little is known, however, about genetic mechanisms of kidney aging. We sought to define the signatures of age on the renal transcriptome using 563 human kidneys. The initial discovery analysis of 260 kidney transcriptomes from the TRANScriptome of renaL humAn TissuE Study (TRANSLATE) and the Cancer Genome Atlas identified 37 age-associated genes. For 19 of those genes, the association with age was replicated in 303 kidney transcriptomes from the Nephroseq resource. Surveying 42 nonrenal tissues from the Genotype-Tissue Expression project revealed that, for approximately a fifth of the replicated genes, the association with age was kidney-specific. Seventy-three percent of the replicated genes were associated with functional or histological parameters of age-related decline in kidney health, including glomerular filtration rate, glomerulosclerosis, interstitial fibrosis, tubular atrophy, and arterial narrowing. Common genetic variants in four of the age-related genes, namely LYG1, PPP1R3C, LTF and TSPYL5, correlated with the trajectory of age-related changes in their renal expression. Integrative analysis of genomic, epigenomic, and transcriptomic information revealed that the observed age-related decline in renal TSPYL5 expression was determined both genetically and epigenetically. Thus, this study revealed robust molecular signatures of the aging kidney and new regulatory mechanisms of age-related change in the kidney transcriptome.
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.