Evidence map›Paper›PMID 37987887›Full record

ArticleGeroScience2024

Heterogeneity of increased biological age in type 2 diabetes correlates with differential tissue DNA methylation, biological variables, and pharmacological treatments.

Briana N Cortez, Hui Pan, Samuel Hinthorn, Han Sun, Nicola Neretti, Anna L Gloyn, Cristina Aguayo-Mazzucato

Open access · greenAbstract read
In one paragraph

Article in GeroScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.5field-weighted citation impact, top 17% of its field
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

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
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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

7 authors at 3 institutions in 1 country.

Briana N CortezJoslin Diabetes Center, Harvard Medical School, Boston, MA, USA.ORCID 0000-0002-5222-5661
Hui PanJoslin Diabetes Center, Harvard Medical School, Boston, MA, USA.ORCID 0000-0001-5748-7217
Samuel HinthornDepartment of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI, 02912, USA.ORCID 0000-0001-6403-6852
Han SunDivision of Endocrinology, Department of Pediatrics, Stanford School of Medicine, Stanford University, Stanford, CA, USA.ORCID 0000-0002-3390-0027
Nicola NerettiDepartment of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI, 02912, USA.ORCID 0000-0002-9552-1663
Anna L GloynDivision of Endocrinology, Department of Pediatrics, Stanford School of Medicine, Stanford University, Stanford, CA, USA.ORCID 0000-0003-1205-1844
Cristina Aguayo-MazzucatoJoslin Diabetes Center, Harvard Medical School, Boston, MA, USA. cristina.aguayo-mazzucato@joslin.harvard.edu.ORCID 0000-0001-5402-1382
Joslin Diabetes Center · USBrown University · USStanford University · US

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 1986 to 2026
$50.5M
Elucidating and targeting beta-cell senescence and its SASPR01DK132535 · NIDDK · JOSLIN DIABETES CENTER · PI Cristina Aguayo-Mazzucato · 2022 to 2026
$2.1M
Spatial omics technologies to map the senescent cell microenvironmentUG3CA268202 · NCI · BROWN UNIVERSITY · PI MA, JIAN, NERETTI, NICOLA · 2021 to 2022
$916k
NCI NIH HHS UG3 CA268202NIDDK NIH HHS P30 DK036836NIDDK NIH HHS R01 DK132535Wellcome Trust 095101Wellcome Trust 200837
6 · The paper itself

Abstract

Biological age (BA) closely depicts age-related changes at a cellular level. Type 2 diabetes mellitus (T2D) accelerates BA when calculated using clinical biomarkers, but there is a large spread in the magnitude of individuals' age acceleration in T2D suggesting additional factors contributing to BA. Additionally, it is unknown whether BA can be changed with treatment. We hypothesized that potential determinants of the heterogeneous BA distribution in T2D could be due to differential tissue aging as reflected at the DNA methylation (DNAm) level, or biological variables and their respective therapeutic treatments. Publicly available DNAm samples were obtained to calculate BA using the DNAm phenotypic age (DNAmPhenoAge) algorithm. DNAmPhenoAge showed age acceleration in T2D samples of whole blood, pancreatic islets, and liver, but not in adipose tissue or skeletal muscle. Analysis of genes associated with differentially methylated CpG sites found a significant correlation between eight individual CpG methylation sites and gene expression. Clinical biomarkers from participants in the NHANES 2017-2018 and ACCORD cohorts were used to calculate BA using the Klemera and Doubal (KDM) method. Cardiovascular and glycemic biomarkers associated with increased BA while intensive blood pressure and glycemic management reduced BA to CA levels, demonstrating that accelerated BA can be restored in the setting of T2D.

Indexed as

Diabetes Mellitus, Type 2DNA MethylationAgingBiomarkersDNAEpigenesis, GeneticHumansNutrition SurveysBiomarkersDNABiological agingType 2 diabetes

Identifiers

PMID37987887
PMCPMC10828255
OpenAlexW4388865818

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.