Evidence map›Paper›PMID 38488948›Full record

ReviewGeroScience2024

Somatic mutations in aging and disease.

Peijun Ren, Jie Zhang, Jan Vijg

Open access · greenAbstract readReview
In one paragraph

Review in GeroScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

22 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Somatic mutations and genome mosaicism in aging and disease.Experimental & molecular medicine · 2026
    Review
  3. Somatic mutation analysis of mucin genes and pathways in idiopathic pulmonary fibrosis.American journal of respiratory and critical care medicine · 2026
    Article
  4. Article
  5. The aging genome exhibits organized vulnerability to somatic mutations.bioRxiv : the preprint server for biology · 2026
    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

3 authors at 2 institutions in 2 countries.

Peijun Ren *Center for Single-Cell Omics, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China. pjren@shsmu.edu.cn.ORCID 0000-0001-6082-945X
Jie Zhang *Center for Single-Cell Omics, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Jan VijgCenter for Single-Cell Omics, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China. jan.vijg@einsteinmed.edu.
Shanghai Jiao Tong University · CNAlbert Einstein College of Medicine · US

Funding

THE IMPACT OF CELLULAR DEFENSE ON THE ROLE OF Ku80 IN GENOME MAINTENANCE AND LONGP01AG017242 · NIA · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI VIJG, JAN · 1999 to 2023
$46.1M
The role of hyaluronan in longevity and cancer resistance of longest-lived rodentP01AG047200 · NIA · UNIVERSITY OF ROCHESTER · PI Vadim N. Gladyshev · 2014 to 2026
$36.9M
Validation and characterization of the identified variants associated with human longevity in mouse modelsU19AG056278 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI JAN VIJG · 2017 to 2026
$24.5M
DOD grant BC180689P1National Natural Science Foundation of China 82172461NIA NIH HHS P01 AG017242NIA NIH HHS P01 AG047200NIA NIH HHS U19 AG056278NIH HHS AG017242NIH HHS AG038072NIH HHS AG047200NIH HHS AG056278NIH HHS ES029519NIH HHS HL145560
6 · The paper itself

Abstract

Time always leaves its mark, and our genome is no exception. Mutations in the genome of somatic cells were first hypothesized to be the cause of aging in the 1950s, shortly after the molecular structure of DNA had been described. Somatic mutation theories of aging are based on the fact that mutations in DNA as the ultimate template for all cellular functions are irreversible. However, it took until the 1990s to develop the methods to test if DNA mutations accumulate with age in different organs and tissues and estimate the severity of the problem. By now, numerous studies have documented the accumulation of somatic mutations with age in normal cells and tissues of mice, humans, and other animals, showing clock-like mutational signatures that provide information on the underlying causes of the mutations. In this review, we will first briefly discuss the recent advances in next-generation sequencing that now allow quantitative analysis of somatic mutations. Second, we will provide evidence that the mutation rate differs between cell types, with a focus on differences between germline and somatic mutation rate. Third, we will discuss somatic mutational signatures as measures of aging, environmental exposure, and activities of DNA repair processes. Fourth, we will explain the concept of clonally amplified somatic mutations, with a focus on clonal hematopoiesis. Fifth, we will briefly discuss somatic mutations in the transcriptome and in our other genome, i.e., the genome of mitochondria. We will end with a brief discussion of a possible causal contribution of somatic mutations to the aging process.

Indexed as

AgingMutationAnimalsDNA RepairHigh-Throughput Nucleotide SequencingHumansMiceMutation RateAgingCancerMutational signaturesSingle-cell whole genome sequencingSingle-molecule sequencingSomatic mutation

Identifiers

PMID38488948
PMCPMC11336144
OpenAlexW4392863093

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.