Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Failure to Repair Endogenous DNA Damage in β-Cells Causes Adult-Onset Diabetes in Mice

26 Oct 2023

Abstract excerpt

Age is the greatest risk factor for the development of type 2 diabetes mellitus (T2DM).Age-related decline in organ function is attributed to the accumulation of stochastic damage, including damage to the nuclear genome.Islets of T2DM patients display increased levels of DNA damage.However, whether this is a cause or consequence of the disease has not been elucidated.Here, we asked if spontaneous, endogenous DNA...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Diet and metabolism studies
Share to DNA Repair Mechanisms
Share to Pancreatic function and diabetes

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 38124711
DOI: 10.59368/agingbio.20230015

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Failure to Repair Endogenous DNA Damage in β-Cells Causes Adult-Onset Diabetes in MicePMID 38124711Read ↗

DNA damage to β cells in culture recapitulates features of senescent β cells that accumulate in type 1 diabetesSemantic proximity Read ↗

Spontaneous DNA damage to the nuclear genome promotes senescence, redox imbalance and agingSemantic proximity Read ↗

DNA damage models phenotypes of β cell senescence in Type 1 DiabetesSemantic proximity Read ↗

Absence of p53-dependent apoptosis combined with nonhomologous end-joining deficiency leads to a severe diabetic phenotype in mice.Semantic proximity Read ↗

Developmental control of DNA damage responses in α- and β-cells shapes the selective beta-cell susceptibility in diabetesSemantic proximity Read ↗

Single cell transcriptome analysis of human pancreas reveals transcriptional signatures of aging and somatic mutation patternsSemantic proximity Read ↗

Too many breaks (brakes): Pancreatic β-cell senescence leads to diabetesSemantic proximity Read ↗

DNA repair in cardiomyocytes is critical for maintaining cardiac function in miceSemantic proximity Read ↗

The Transcription Factor YY1 Is Essential for Normal DNA Repair and Cell Cycle in Human and Mouse β-CellsSemantic proximity Read ↗

KAT2B Is Required for Pancreatic Beta Cell Adaptation to Metabolic Stress by Controlling the Unfolded Protein ResponseSemantic proximity Read ↗

Cisplatin exposure dysregulates pancreatic islet function in male miceSemantic proximity Read ↗

The pancreatic β-cell in ageing: Implications in age-related diabetesSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.