Evidence mapPaperPMID 41604428Full record

ArticleCardiovascular research2026

Shorter kidney telomeres are associated with nephrosclerosis by an epigenetic signature.

Olutope Arinola Akinnibosun, Xiaoguang Xu, Amber Emmett, Huy Nguyen, Shadi Hames-Fathi, Maciej Drzal, James Eales, David Scannali, Priscilla R Prestes, Matthew Denniff and 9 more

Abstract read
In one paragraph

Article in Cardiovascular research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

19 authors.

Olutope Arinola AkinnibosunHealth Innovation and Transformation Centre, Federation University Australia, Ballarat, Y building, University Drive, Ballarat, VIC 3353, Australia.ORCID 0000-0001-8113-4454
Xiaoguang XuDivision of Cardiovascular Sciences, Faculty of Medicine, Biology and Health, University of Manchester, Upper Brook Street, Manchester M13 9PT, UK.ORCID 0000-0003-4568-1623
Amber EmmettDivision of Cardiovascular Sciences, Faculty of Medicine, Biology and Health, University of Manchester, Upper Brook Street, Manchester M13 9PT, UK.
Huy NguyenHealth Innovation and Transformation Centre, Federation University Australia, Ballarat, Y building, University Drive, Ballarat, VIC 3353, Australia.
Shadi Hames-FathiDivision of Cardiovascular Sciences, Faculty of Medicine, Biology and Health, University of Manchester, Upper Brook Street, Manchester M13 9PT, UK.
Maciej DrzalDivision of Cardiovascular Sciences, Faculty of Medicine, Biology and Health, University of Manchester, Upper Brook Street, Manchester M13 9PT, UK.
James EalesDivision of Cardiovascular Sciences, Faculty of Medicine, Biology and Health, University of Manchester, Upper Brook Street, Manchester M13 9PT, UK.ORCID 0000-0001-6238-5952
David ScannaliDivision of Cardiovascular Sciences, Faculty of Medicine, Biology and Health, University of Manchester, Upper Brook Street, Manchester M13 9PT, UK.ORCID 0000-0002-0580-4003
Priscilla R PrestesHealth Innovation and Transformation Centre, Federation University Australia, Ballarat, Y building, University Drive, Ballarat, VIC 3353, Australia.
Matthew DenniffDepartment of Cardiovascular Sciences, University of Leicester, Leicester LE1 7RH, UK.
Pawel BogdanskiDepartment of Obesity, Metabolic Disorders Treatment and Clinical Dietetics, Karol Marcinkowski University of Medical Sciences, Poznan 61-701, Poland.ORCID 0000-0002-0563-1624
Joanna ZywiecDepartment of Internal Medicine, Diabetology and Nephrology, Zabrze, Medical University of Silesia, Katowice 40-055, Poland.ORCID 0000-0002-0661-8157
Wojciech WystrychowskiDepartment of General, Vascular and Transplant Surgery, Faculty of Medical Sciences in Katowice, Medical University of Silesia, Katowice, Poland.ORCID 0000-0002-2430-1225
Ewa Zukowska-SzczechowskaDepartment of Health Care, Silesian Medical College, Katowice 40-752, Poland.
Tomasz J GuzikDepartment of Internal Medicine, Jagiellonian University Medical College, Kraków 31-0008, Poland.
Nilesh J SamaniDepartment of Cardiovascular Sciences, University of Leicester, Leicester LE1 7RH, UK.
John DormerDepartment of Cellular Pathology, University Hospitals of Leicester, Leicester LE5 4PW, UK.ORCID 0000-0001-7615-6149
Maciej TomaszewskiDivision of Cardiovascular Sciences, Faculty of Medicine, Biology and Health, University of Manchester, Upper Brook Street, Manchester M13 9PT, UK.ORCID 0000-0001-8215-6567
Fadi J CharcharHealth Innovation and Transformation Centre, Federation University Australia, Ballarat, Y building, University Drive, Ballarat, VIC 3353, Australia.

Funding

Australian Government Regional Research CollaborationBritish Heart Foundation PG/17/35/33001British Heart Foundation PG/19/16/34270British Heart Foundation PG/22/10957British Heart Foundation Manchester Research Excellence Award RE/24/130017Destination Australia ScholarshipManchester Biomedical Research Centre NIHR203308National Institute for Health and Care ResearchNational Institute for Health and Care Research Manchester Biomedical Research NIHR203308
6 · The paper itself

Abstract

aimsAgeing leads to a progressive loss in structural integrity and a functional decline of human organs, alongside telomere attrition and alterations in DNA methylation patterns. Their relationships in the human kidney in the context of ageing remain elusive. METHODS AND

resultsWe analysed 200 participants from the human kidney tissue resource (HKTR) with matching information on kidney histology, renal function, blood leucocyte and kidney telomere length, as well as kidney genome-wide DNA methylation profiles. Additional 71 HKTR individuals without telomere data were used in validation analyses. Kidney telomere length showed a significant inverse association with age (β = -0.029, confidence interval = -0.043 to -0.016, P = 0.00003). Shorter kidney telomeres were strongly associated with both renal structure and function, independent of demographic and clinical confounders. Nephrosclerosis score showed a gradual increase with age categories, whilst kidney telomere length dropped simultaneously. Leucocyte telomere length was not related to the extent of age-related changes in kidney function or structure. Kidney DNA methylation analysis revealed that kidney CpGs, genes, pathways, and chromatin patterns associated with kidney telomere length are partly independent of these associated with chronological age. Consisted of 57 CpGs, epigenetic clock of kidney telomere length showed a predictive potential for nephrosclerosis, independent of clinical cofounders, chronological, and epigenetic age.

conclusionOur study revealed that gradual age-related structural involution of human kidney and a decline in its filtration capacity are accompanied by shortening of telomeres in renal cells and that changes in the kidney epigenome (i.e. DNA methylation) may contribute to nephrosclerosis (at least in part) independently of chronological age.

Indexed as

AgingDNA MethylationEpigenesis, GeneticKidneyNephrosclerosisTelomereTelomere ShorteningAdultAgedAged, 80 and overAge FactorsCpG IslandsFemaleGenetic Predisposition to DiseaseHumansMaleEpigeneticsKidney ageingNephrosclerosisRenal fibrosisTelomere

Identifiers

PMID41604428
PMCPMC13020538

What Socratic holds

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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.